EMDR: A putative neurobiological mechanism of action
Article first published online: 12 DEC 2001
Copyright © 2002 John Wiley & Sons, Inc.
Journal of Clinical Psychology
Volume 58, Issue 1, pages 61–75, January 2002
How to Cite
Stickgold, R. (2002), EMDR: A putative neurobiological mechanism of action. J. Clin. Psychol., 58: 61–75. doi: 10.1002/jclp.1129
- Issue published online: 12 DEC 2001
- Article first published online: 12 DEC 2001
Numerous studies have provided evidence for the efficacy of eye movement desensitization and reprocessing therapy (EMDR) in the treatment of posttraumatic stress disorder (PTSD), including recent studies showing it to be more efficient than therapist-directed flooding. But few theoretical explanations of how EMDR might work have been offered. Shapiro, in her original description of EMDR, proposed that its directed eye movements mimic the saccades of rapid eye movement sleep (REM), but provided no clear explanation of how such mimicry might lead to clinical improvement. We now revisit her original proposal and present a complete model for how EMDR could lead to specific improvement in PTSD and related conditions. We propose that the repetitive redirecting of attention in EMDR induces a neurobiological state, similar to that of REM sleep, which is optimally configured to support the cortical integration of traumatic memories into general semantic networks. We suggest that this integration can then lead to a reduction in the strength of hippocampally mediated episodic memories of the traumatic event as well as the memories' associated, amygdala-dependent, negative affect. Experimental data in support of this model are reviewed and possible tests of the model are suggested. © 2002 John Wiley & Sons, Inc. J Clin Psychol 58: 61–75, 2002.