Eye movement desensitization and reprocessing as a treatment for PTSD: current neurobiological theories and a new hypothesis.
Eye movement desensitization and reprocessing (EMDR), a form of psychotherapy for individuals with post-traumatic stress disorder (PTSD), has long been a controversial topic, hampered in part by a lack of understanding of the neural mechanisms that contribute to its remedial effect. Here, we review current theories describing EMDR's potential neurobiological mechanisms of action involving working memory, interhemispheric communication, de-arousal, and memory reconsolidation. We then discuss recent studies describing the temporal and spatial aspects of smooth pursuit and predictive saccades, which resemble those made during EMDR, and their neural correlates within the default mode network (DMN) and cerebellum. We hypothesize that if the production of bilateral predictive eye movements is supportive of DMN and cerebellum activation, then therapies that shift the brain towards this state correspondingly would benefit the processes regulated by these structures (i.e., memory retrieval, relaxation, and associative learning), all of which are essential components for PTSD recovery. We propose that the timing of sensory stimulation may be relevant to treatment effect and could be adapted across different patients depending on their baseline saccade metrics. Empirical data in support of this model are reviewed and experimental predictions are discussed.