Abstract
Since the seminal report by Shapiro that bilateral stimulation induces cognitive and emotional changes, 26 years of basic and clinical research have examined the effects of Eye Movement Desensitization and Reprocessing (EMDR) in anxiety disorders, particularly in post-traumatic stress disorder (PTSD). The present article aims at better understanding EMDR neural mechanism. I first review procedural aspects of EMDR protocol and theoretical hypothesis about EMDR effects, and develop the reasons why the scientific community is still divided about EMDR. I then slide from psychology to physiology describing eye movements/emotion interaction from the physiological viewpoint, and introduce theoretical and technical tools used in movement research to re-examine EMDR neural mechanism. Using a recent physiological model for the neuropsychological architecture of motor and cognitive control, the Threshold Interval Modulation with Early Release-Rate of rIse Deviation with Early Release (TIMER-RIDER)—model, I explore how attentional control and bilateral stimulation may participate to EMDR effects. These effects may be obtained by two processes acting in parallel: (i) activity level enhancement of attentional control component; and (ii) bilateral stimulation in any sensorimotor modality, both resulting in lower inhibition enabling dysfunctional information to be processed and anxiety to be reduced. The TIMER-RIDER model offers quantitative predictions about EMDR effects for future research about its underlying physiological mechanisms.
Highlights
In 1987, Francine Shapiro observed on herself that rhythmic eye movements may cause cognitive and emotional changes
As developed in ‘‘Procedural aspects’’ Section, the Eye Movement Desensitization and Reprocessing (EMDR) protocol involves at least eight components, but the only distinctive feature as compared to other Cognitive and Behavioral Therapy (CBT) treatments is the therapistinduced bilateral stimulation (Cahill et al, 1999). This issue has been addressed in several studies in PostTraumatic Stress Disorder (PTSD)/trauma (e.g., Devilly et al, 1998) and other anxiety disorders such as simple phobia (e.g., Sanderson and Carpenter, 1992), but to date it remains controversial whether eye movements or other laterally alternating stimuli play a role in EMDR effects (Lilienfeld, 1996/2011; Herbert et al, 2000; Davidson and Parker, 2001; Servan-Schreiber et al, 2006; van den Hout et al, 2012)
The authors showed that the anterior cingulate cortex (ACC) activity was positively correlated to the distance to the decisional threshold, but not to the slope of the accumulation of sensory evidence, whereas the right dorsolateral prefrontal cortex (DLPFC) showed the reverse pattern, i.e., was positively correlated to the decision gain but not to the distance to the decisional threshold (Domenech and Dreher, 2010)
Summary
In 1987, Francine Shapiro observed on herself that rhythmic eye movements may cause cognitive and emotional changes From that observation, she developed a Cognitive and Behavioral Therapy (CBT)-inspired protocol called Eye Movement Desensitization and Reprocessing (EMDR; initially EMD EMDR) to treat anxiety disorders, PostTraumatic Stress Disorder (PTSD; Shapiro, 1989a,b). She developed a Cognitive and Behavioral Therapy (CBT)-inspired protocol called Eye Movement Desensitization and Reprocessing (EMDR; initially EMD EMDR) to treat anxiety disorders, PostTraumatic Stress Disorder (PTSD; Shapiro, 1989a,b) In this protocol, left-right smooth pursuit eye movements are elicited to alleviate negative cognition, negative emotion, and unpleasant physical sensations associated with a traumatic memory (desensitization phase) and to reinforce positive cognition (reprocessing phase). I will present theoretical and technical tools currently used in movement research, and explore how such quantitative tools may help to put forth our understanding of EMDR neural mechanism
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