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What does the research show about the neurobiological aspects of EMDR?

Given the infancy of the field of neurobiology, the physiological foundations of all psychotherapies are currently unknown, and therefore, all neurobiological models of psychotherapy are speculative. Testing of hypotheses about the neurological mechanisms of any form of psychotherapy and most pharmaceuticals awaits the development of advanced brain imaging techniques. Hypotheses concerning EMDR’s neurobiological mechanisms are, at this time, purely speculative.

Rauch, van der Kolk, and colleagues (1996) conducted positron emission studies of patients with PTSD in which they were exposed to vivid, detailed narratives which they had written about their own traumatic experiences. Patients showed heightened activity only in the right hemisphere, in the areas most involved in emotional arousal, and heightened activity on the right visual cortex, reflecting the flashbacks reported by these patients. Perhaps most significantly, Broca’s area - the part of the left hemisphere responsible for translating personal experiences into communicable language -“turned off”. These findings indicate that PTSD symptoms are reflected in actual changes in brain activity.

Case study research by van der Kolk and colleagues (Levin, Lazrove, & van der Kolk, 1999; van der Kolk, Burbridge, & Suzuki, 1997; Zoler, 1998) has provided some preliminary evidence that changes in brain activation patterns may follow effective treatment. SPECT scans were administered pre and post-EMDR for 6 PTSD subjects who each received 3 EMDR sessions. The Zoler article has photos of pre and post SPECT scans. Findings indicated metabolic changes after EMDR in two specific brain regions. First, there was an increase in bilateral activity of the anterior cyngulate. This area moderates the experience of real versus perceived threat, indicating that after EMDR, PTSD sufferers may no longer be hypervigilant. Second, there appeared to be an increase in pre-frontal lobe metabolism. An increase in frontal lobe functioning may indicate improvement in the ability to make sense of incoming sensory stimulation. Levin et al. concluded that EMDR appeared to facilitate information processing. Because there was no control group, there is no evidence that these effects were unique to EMDR; effective treatment of any kind may produce similar results.

Lansing, K., Amen, D.G., Hanks, C. & Rudy, L. (2005) reported that pre- post treatment SPECT scans indicated a decrease in anterior cingulate, basal ganglia and deep limbic activity. The 12th chapter of Shapiro’s (2001) text details some related recent neurological research and explains the possible relevance of these findings to EMDR. Also of interest is an article by Stickgold (2002), a sleep researcher, who has developed a theory to explain the effects of EMDR’s alternating, bilateral stimulation which forces the client to constantly shift his or her attention across the midline. He proposed that REM-like neurobiological mechanisms are facilitated by this shifting attention, resulting in the activation of episodic memories, and their integration into cortical semantic memory. Independent research by Christman, S. D., Garvey, K. J., Propper, R. E., & Phaneuf, K. A. (2003) provides some support for this theory. They determined that alternating leftward and rightward eye movements produced a beneficial effect for episodic, but not semantic, retrieval memory tasks.  See also Kuiken et al., 2002, 2010  (Research Overview)

All psychophysiological studies have indicated significant de-arousal. Neurobiological studies have indicated significant effects, including changes in cortical, and limbic activation patterns, and increase in hippocampal volume. 

Aubert-Khalfa, S., Roques, J. & Blin, O. (2008). Evidence of a decrease in heart rate and skin conductance responses in PTSD patients after a single EMDR session. Journal of EMDR Practice and Research, 2, 51-56.

Bossini L. Fagiolini, A. & Castrogiovanni, P. (2007). Neuroanatomical changes after EMDR in posttraumatic stress disorder. Journal of Neuropsychiatry and Clinical Neuroscience, 19, 457-458.

Bossini, L., Tavanti, M., Calossi, S., Polizzotto, N. R., Vatti, G., Marino, D., & Castrogiovanni, P. (2011). EMDR treatment for posttraumatic stress disorder, with focus on hippocampal volumes: A pilot study. The Journal of Neuropsychiatry and Clinical Neurosciences, 23, E1-2. doi:10.1176/appi. neuropsych.23.2.E1

Frustaci, A., Lanza, G.A., Fernandez, I., di Giannantonio, M. & Pozzi, G. (2010). Changes in psychological symptoms and heart rate variability during EMDR treatment: A case series of subthreshold PTSD. Journal of EMDR Practice and Research, 4, 3-11.

Grbesa et al. (2010). Electrophysiological changes during EMDR treatment in patients with combat-related PTSD. Annals of General Psychiatry 9 (Suppl 1):S209.

Harper, M. L., Rasolkhani-Kalhorn, T., & Drozd, J. F. (2009). On the neural basis of EMDR therapy: Insights from qeeg studies. Traumatology, 15, 81-95.

Kowal, J. A. (2005). QEEG analysis of treating PTSD and bulimia nervosa using EMDR. Journal of Neurotherapy, 9 (Part 4), 114-115.

Lamprecht, F., Kohnke, C., Lempa, W., Sack, M., Matzke, M., & Munte, T. (2004). Event-related potentials and EMDR treatment of post-traumatic stress disorder. Neuroscience Research, 49, 267-272.

Landin-Romero, R., et al. (2013). EMDR therapy modulates the default mode network in a subsyndromal, traumatized bipolar patient. Neuropsychobiology, 67, 181-184.

Lansing, K., Amen, D.G., Hanks, C. & Rudy, L. (2005). High resolution brain SPECT imaging and EMDR in police officers with PTSD. Journal of Neuropsychiatry and Clinical Neurosciences, 17, 526-532.

Levin, P., Lazrove, S., & van der Kolk, B. A. (1999). What psychological testing and neuroimaging tell us about the treatment of posttraumatic stress disorder (PTSD) by eye movement desensitization and reprocessing (EMDR). Journal of Anxiety Disorders, 13, 159-172.

Nardo D et al. (2010). Gray matter density in limbic and paralimbic cortices is associated with trauma load and EMDR outcome in PTSD patients. Journal of Psychiatric Research, 44, 477-485.

Oh, D.-H., & Choi, J. (2004). Changes in the regional cerebral perfusion after eye movement desensitization and reprocessing: A SPECT study of two cases. Journal of EMDR Practice and Research, 1, 24-30.

Ohta ni, T., Matsuo, K., Kasai, K., Kato, T., & Kato, N. (2009). Hemodynamic responses of eye movement desensitization and reprocessing in posttraumatic stress disorder. Neuroscience Research, 65, 375–383.

Pagani, M. et al. (2007). Effects of EMDR psychotherapy on 99mTc-HMPAO distribution in occupation-related post-traumatic stress disorder. Nuclear Medicine Communications, 28, 757–765.

Pagani, M. et al. (2011). Pretreatment, intratreatment, and posttreatment EEG imaging of EMDR: Methodology and preliminary results from a single case. Journal of EMDR Practice and Research, 5, 42-56.

Pagani, M. et al. (2012). Neurobiological correlates of EMDR monitoring – An EEG study. PLoS ONE, 7(9) e45753 doi:10.1371/journal.pone.0045753

Propper, R., Pierce, J.P., Geisler, M.W., Christman, S.D., & Bellorado, N. (2007). Effect of bilateral eye movements on frontal interhemispheric gamma EEG coherence: Implications for EMDR therapy. Journal of Nervous and Mental Disease, 195, 785-788.

Richardson, R., Williams, S.R., Hepenstall, S., Gregory, L., McKie, S. & Corrigan, F. (2009). A single-case fMRI study: EMDR treatment of a patient with posttraumatic stress disorder. Journal of EMDR Practice and Research, 3, 10-23.

Sack, M., Lempa, W., & Lemprecht, W. (2007). Assessment of psychophysiological stress reactions during a traumatic reminder in patients treated with EMDR. Journal of EMDR Practice and Research, 1, 15-23.

Sack, M., Nickel, L., Lempa, W., & Lamprecht, F. (2003) Psychophysiological regulation in patients suffering from PTSD: Changes after EMDR treatment. Journal of Psychotraumatology and Psychological Medicine, 1, 47 -57. (German)

van der Kolk, B., Burbridge, J., & Suzuki, J. (1997). The psychobiology of traumatic memory: Clinical implications of neuroimaging studies. Annals of the New York Academy of Sciences, 821, 99-113.