First and foremost, nothing, with respect to the neurobiology of EMDR, has been in any way proven. The only data that exists comes from van der Kolk et al. S.P.E.C.T. scan study of EMDR treatment, published in 1997 and 1999. In this study, following succesful EMDR treatment subjects no longer met criteria for PTSD as per symptoms and psychometric measures. Neuroimaging revealed that upon recall of the traumatic memory, 2 areas of the brain evidenced increased activation, post-EMDR treatment relative to pre-EMDR treatment: the frontal area and the anterior cingulate gyrus. In addition to this, there are some intersting ideas out there and 2 speculative models which are beginning to cohere, theoretically, grounded by solid laboratory and neuroimaging studies from related areas and fields. Robert Stickgold's very elegant model posits that the repetitive redirecting of attention in EMDR (EMs, tactile and auditory), facilitates a constant neurological startle, driving a constant surge of Acetylcholine. This cholinergic surge is capable of turning on the brain's REM sleep system, leading to the activation of certain areas of the the anterior cortex of the cingulate gyrus, facilitating its function as a filter, thereby facilitating the integration of traumatic memory into general semantic memory networks. This integration is seen to lead to the subsequent reduction in strength of both hippocampally mediated episodic memories of the traumatic event as well as the amygdaloid mediated negative affect of PTSD. This also facilitates the processing of implicit (non-verbal) memory networks (experienced as somatosensory), which are suspected to be amygdaloid mediated. The other modal, which I have submitted for publication, elaborates the mediation of the cerebellum in EMDR processing. It posits that EMDR (EMs, tactile and auditory) stimulation is also a constant sensory stimulation. The cerebellum receives input and is activated from virtually every sensory system, including vestibular, proprioceptive, visual, auditory, tactile and somatosensory. More than a decade of laboratory research has shown that the cerebellum can serve as a link between the posterior and frontal language areas of the cerebral neocortex. In effect, the neocerebellum has been shown to provide the cerebral cortex with an additional 'association area'. Supporting this view, is the recent behavioral and empirical evidence that the cerebellum participates in cognitive and language functions of the human brain, beyond the purely motor expression of speech or gesture. Such evidence has, also, emerged as a result of advanced techniques for scanning and imaging the brain which have revealed that the lateral cerebellum is strikingly activated when an individual performs information-processing, semantic association, working memory, declarative and episodic memory tasks. Anatomical and cell studies have shown that the activation of the dentate nuclei in the lateral neocerebellum is shown to facilitate activation of the ventrolateral and central lateral thalamic nuclei. The activation of the central lateral thalamic nucleus has been shown to activate the hypothalamus and hence the limbic strucures. The activation of the ventrolateral nucleus is shown to lead to the activation of the prefrontal cortex (comprised of the orbitofrontal and dorsolateral cortices) in general, and Broca's Language Area, specifically. These findings compliment Stickgold's model, because in REM-sleep the left dorsolateral verbal and executive areas are inactive. This cerebellar mediation begins to explain, how in addition to activating REM systems, EMDR activates frontal areas, already seen in neuroimaging of EMDR, further facilitating the integration of traumatic memory into general semantic and other neocortical networks. In neither of these modals is EMDR stim seen as bilaterally necessary. In Stickgold's it is a "redirecting of attention". That's probably why EMDR can be done with vertical EMs. In my modal it is a constant sensory input. All of this PROVES nothing, but begins to speculate, in a grounded way, that bilaterality may not be a factor. They also illustrate, speculatively, why eye movements, alternating audio and tactile stimulation have been seen to be equivalent with respect to our experiences with EMDR for the past 10 years. Both modals will, hopefully, be examined in present and future neuroimaging studies. Hope this helps.
Replies:
![]() |
| Behavior OnLine Home Page | Disclaimer |
Copyright © 1996-2004 Behavior OnLine, Inc. All rights reserved.