2013 EMDR Research Review by Adler-Tapia


author:  Robbie Adler-Tapia, Ph.D.

I. There are more than 30 Randomized Clinical Trials on EMDR including:

van der Kolk, B., Spinazzola, J. Blaustein, M., Hopper, J. Hopper, E., Korn, D., & Simpson, W. (2007). A randomized clinical trial of EMDR, fluoxetine and pill placebo in the treatment of PTSD: Treatment effects and long-term maintenance. Journal of Clinical Psychiatry, 68, 37-46.

For more information:  

            EMDR Institute:  www.emdr.com

           Andrew Leeds’ website:   http://www.sonomapti.com/aboutemdr/guidelines.html where you can also find major review articles, meta-analyses, RCTs and studies on Psychophysiological and Neurobiological Evaluations. 

            *Dr. Leeds regularly reviews the latest research on EMDR and publishes this for the EMDRIA Community.

II. Please note a few of the meta-analyses of EMDR research:

Bisson, J., & Andrew, M. (2009). Psychological treatment of post-traumatic stress disorder (PTSD). Cochrane Database of Systematic Reviews 2009, Issue 3. Art. No.: CD003388. DOI: 10.1002/14651858.CD003388.pub3. “Trauma focused cognitive behavioural therapy and eye movement desensitisation and reprocessing have the best evidence for efficacy at present and should be made available to PTSD sufferers.” (p. 18)

Lee, C.W., & Cuijpers, P. (2013). A meta-analysis of the contribution of eye movements in processing emotional memories. Journal of Behavior Therapy & Experimental Psychiatry, 44, 231-239.

III. The following organizations recognize EMDR Psychotherapy as evidence based practice:

1. The World Health Organization: http://apps.who.int/iris/bitstream/10665/85119/1/9789241505406_eng.pdf

Altogether, EMDR was effective with a medium effect size (Cohen’s d =.56), and found to be more effective than CBT treatments when comparing effect sizes. The variation in effect sizes between studies was partly explained by both treatment and study methodology factors, including year of publication (more recent studies associated with lower effect sizes), type of informant (parent-child reports associated with higher effect sizes than studies using only child reports), drop-out (more drop-out associated with lower effect sizes), type of comparison (comparison with established treatments associated with lower effect sizes) and number of sessions (fewer sessions associated with higher effect sizes).

2. The Cochrane Collaboration:  http://onlinelibrary.wiley.com/store/10.1002/14651858.CD003388.pub3/asset/CD003388.pdf?v=1&t=hnapo7c3&s=2cb02ff8204df514fd28a420bdccccbc81e0bc0e  

EMDR appeared to have similar effectiveness to TFCBT in the studies that compared them directly. There was some evidence that EMDR was a more effective treatment than stress management therapies and other therapies. (pp. 17).


3. Substance Abuse and Mental Health Services Administration, National Registry of Evidence Based Programs and Practices


4. Department of Defense and Department of Veterans’ Affairs 


5.The US Department of Veterans’ Affairs: National Center for PTSD.


6. NICE:     http://www.nice.org.uk/nicemedia/live/10966/29769/29769.pdf

7.  International Society for Traumatic Stress Studies (ISTSS) 


EMDR is rated as a Level A treatment for its use with adults. Quality clinical trials support its use for patients with PTSD. More studies need to be com-pleted with EMDR adapted for use with children and adolescents. It currently has a Level B rating for treatment with this population. 

 8. American Psychiatric Association: Page 32 references EMDR


American Psychiatric Association (2010) http://psychiatryonline.org/pdfaccess.ashx? ResourceID=243186&PDFSource=6    

In summary, EMDR belongs within a continuum of exposure-related and cognitive behavior treatments. EMDR employs techniques that may give the patient more control over the exposure experience (since EMDR is less reliant on a verbal account) and provides techniques to regulate anxiety in the apprehensive circumstance of exposure treatment. Consequently, it may prove advantageous for patients who cannot tolerate prolonged exposure as well as for patients who have difficulty verbalizing their traumatic experiences. Comparisons of EMDR with other treatments in larger samples are needed to clarify such differences. The dismantling studies, in general, show no incremental effect from the use of eye movement or other proxies during the treatment sessions. Despite the demonstrable efficacy of EMDR, these studies call into question EMDR’s theoretical rationale. It would therefore appear that it is the common sharing of trauma exposure techniques and emotional reprocessing that is principally responsible for treatment gains. Thus, EMDR is better than no treatment or supportive counseling and may be as effective as cognitive behavior therapy and other exposure-based techniques. As with the other therapies, the extent to which gains are maintained over the long term requires further evaluation.

IV.  The Neurophysiological and Neurobiological Mechanisms of EMDR

1. Clinical trials on EMDR AND PE – de Bont et al. Trials 2013, 14:151 http://www.trialsjournal.com/content/14/1/151

A multi-site single blind clinical study to compare the effects of prolonged exposure, eye movement desensitization and reprocessing and waiting list on patients with a current diagnosis of psychosis and co morbid post traumatic stress disorder: study protocol for the randomized controlled trial Treating Trauma in Psychosis.    

Paul AJM de Bont1,2*, David PG van den Berg3,4, Berber M van der Vleugel4,5, Carlijn de Roos6, Cornelis L

Mulder7, Eni S Becker2, Ad de Jongh8,9,10, Mark van der Gaag3,4 and Agnes van Minnen2,11

1. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3667059/  

2. Dr. Uri Bergmann has published a book “Neurobiological Foundations for EMDR Practice” 

3. Dr. Stickgold from the Department of Psychiatry at Harvard Medical School describes the mechanisms for action in EMDR psychotherapy.   http://www.emdr.nl/acrobat/STICKG1.pdf

4. EMDR Therapy Modulates the Default Mode Network in a Subsyndromal, Traumatized Bipolar Patient

Landin-Romero R. · Novo P. · Vicens V. · McKenna P.J. · Santed A. · Pomarol-Clotet E. ·Salgado-Pineda P. · Shapiro F. · Amann B.L.   Neuropsychobiology 2013;67:181-184 (DOI: 10.1159/000346654)


Background: Some functional imaging abnormalities found in bipolar disorder are state related, whereas others persist into euthymia. It is uncertain to what extent these latter changes may reflect continuing subsyndromal affective fluctuations and whether those can be modulated by therapeutic interventions. Method: We report functional magnetic resonance imaging (fMRI) findings during performance of the n-back working memory task in a bipolar patient who showed a marked improvement in subsyndromal affective symptoms after receiving eye movement desensitization and reprocessing (EMDR) therapy in the context of a clinical trial. Results: The patient’s clinical improvement was accompanied by marked changes in functional imaging, as compared to 30 healthy subjects. fMRI changes were noted particularly in deactivation, with failure of deactivation in the medial frontal cortex partially normalizing after treatment. Conclusions: This case supports the potential therapeutic overall benefit of EMDR in traumatized bipolar patients and suggests a possible neurobiological mechanism of action: normalization of default mode network dysfunction.

5. Neurobiological Correlates of EMDR Monitoring – An EEG Study

Marco Pagani1*, Giorgio Di Lorenzo2, Anna Rita Verardo3, Giampaolo Nicolais4, Leonardo Monaco2,

Giada Lauretti3, Rita Russo3, Cinzia Niolu2, Massimo Ammaniti5, Isabel Fernandez3, Alberto Siracusano2


Background: Eye Movement Desensitization and Reprocessing (EMDR) is a recognized first-line treatment for psychological trauma. However its neurobiological bases have yet to be fully disclosed.

Methods: Electroencephalography (EEG) was used to fully monitor neuronal activation throughout EMDR sessions including the autobiographical script. Ten patients with major psychological trauma were investigated during their first EMDR session (T0) and during the last one performed after processing the index trauma (T1). Neuropsychological tests were administered at the same time. Comparisons were performed between EEGs of patients at T0 and T1 and between EEGs of patients and 10 controls who underwent the same EMDR procedure at T0. Connectivity analyses were carried out by lagged phase synchronization.

Results: During bilateral ocular stimulation (BS) of EMDR sessions EEG showed a significantly higher activity on the orbito- frontal, prefrontal and anterior cingulate cortex in patients at T0 shifting towards left temporo-occipital regions at T1. A similar trend was found for autobiographical script with a higher firing in fronto-temporal limbic regions at T0 moving to right temporo-occipital cortex at T1. The comparisons between patients and controls confirmed the maximal activation in the limbic cortex of patients occurring before trauma processing. Connectivity analysis showed decreased pair-wise interactions between prefrontal and cingulate cortex during BS in patients as compared to controls and between fusiform gyrus and visual cortex during script listening in patients at T1 as compared to T0. These changes correlated significantly with those occurring in neuropsychological tests.

Conclusions: The ground-breaking methodology enabled our study to image for the first time the specific activations associated with the therapeutic actions typical of EMDR protocol. The findings suggest that traumatic events are processed at cognitive level following successful EMDR therapy, thus supporting the evidence of distinct neurobiological patterns of brain activations during BS associated with a significant relief from negative emotional experiences.

Citation: Pagani M, Di Lorenzo G, Verardo AR, Nicolais G, Monaco L, et al. (2012) Neurobiological Correlates of EMDR Monitoring – An EEG Study. PLoS ONE 7(9): e45753. doi:10.1371/journal.pone.0045753

Editor: Ulrike Schmidt, Max Planck Institute of Psychiatry, Germany

Received May 20, 2012; Accepted August 24, 2012; Published September 26, 2012

Copyright: ß 2012 Pagani et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

6. Please note the following regarding brain imaging data: High–Resolution Brain SPECT Imaging and Eye Movement Desensitization and Reprocessing in Police Officers With PTSD Karen Lansing, M.F.T, B.C.E.T.S.; Daniel G. Amen, M.D.; Chris Hanks, Ph.D.; Lisa Rudy, B.A. The Journal of Neuropsychiatry and Clinical Neurosciences 2005;17:526-532. doi:10.1176/appi.neuropsych.17.4.526http://neuro.psychiatryonline.org/article.aspx?articleid=102021 The Journal of Neuropsychiatry and Clinical Neurosciences is also a peer-reviewed journal.

V. Insurance company positions on EMDR:

Aetna:            http://www.aetna.com/cpb/medical/data/500_599/0583.html

BC/BS: http://www.bcbsm.com/newsletter/providernews/archive/2011/05/2011_05_MedicalPolicyUpdates.pdf 

Eye movement desensitization and reprocessing for post traumatic stress disorder

• New policy

• Effective date: Sept. 1, 2011

• Plan approval with clinical review required • Procedure code: *90899

Eye movement desensitization and reprocessing (EMDR) therapy is a behavioral health intervention for post traumatic stress disorder. The EMDR techniques used by a therapist assist the patient in processing traumatic memories in order to resolve them.

EMDR is different from other forms of treatment in that it uses dual stimulation of the brain, such as eye movement or other forms of rhythmical stimulation (for example, sound and touch) to stimulate the brain’s information processing system. During EMDR therapy, the patient recalls memories of traumatic events or triggers while focusing on an outside stimulus, such as the therapist’s finger moving back and forth or repetitive tapping. This technique generally guides the patient to gain new insight associated with the traumatic experience and enables him or her to manage it more effectively.

Eye movement desensitization and reprocessing is an established therapy for adult onset post traumatic stress disorder and may be a covered service for BCN members when indicated. 

Also please check on EMDRIA for additional insurance companies.  Www.emdria.org  Please note that not all of the links on the EMDRIA site are still valid. This document section of the EMDRIA site needs updated.



Neurophysiological Mechanisms of EMDR Psychotherapy.

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.

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.


Robbie Adler-Tapia, Ph.D.


EMDRIA Therapist Certified in EMDR

EMDRIA Approved Consultant and Specialty Trainer

EMDR Institute Facilitator

EMDR/HAP Trainer

1615 E. Warner Road, Suite 2

Tempe, AZ 85284