EMDR FORUM ARCHIVE, 2000
Re: differential mechanism
Ulrich Lanius · 11/01/01 at 8:13 PM ET
Shawn: Thank you for the detailed response. I will focus on the areas where I don't concur. **In the case of EMDR, there are at least three features of the procedure that are (or at least one time were) so integral to the procedure that they were specified in the name: eye movements, desensitization (read exposure), and reprocessing (read installation trials).** The R for Reprocessing, as you probably are aware, was added later, as Shapiro felt that desensitization inadequately accounted for the treatment effect in EMDR, though it was my impression that this was not limited to the actual intallation phase of the treatment. Incidentally, the term reprocessing is also used in CBT (e.g. Rothbaum). **Dismantling studies have shown that eye movements are not necessary. They have also shown that bi-lateral stimulation of other sorts are also not necessary: one can do "EMDR" with eyes fixed and without replacing it with some other form of laterally alternating stimuli and still get comparable outcome.** From my point of view the dismantling studies are not convincing. The major problem here is that the so-called control condition of eye fixation actually evokes similar patterns of brain activation as eye-movements (see Corbetta M, Akbudak E, Conturo TE, Snyder AZ, Ollinger JM, Drury HA, Linenweber MR, Petersen SE, Raichle ME, Van Essen DC, Shulman GL. 1998. A common network of functional areas for attention and eye movements. Neuron, 21: 761-73.) Shapiro tries to account for this in the recent revision of her textbook my referring to dual attention rather than bilateral stimulation. Further with regard to bilateral stimulation, the types of sensory stimulation that are used (visual, auditory, tactile) are certain to affect thalamic activity. There is recent evidence that the latter is impaired during recall of traumatic memories (see Lanius RA, Williamson PC, Densmore M, Boksman K, Gupta MA, Neufeld RW, Gati JS, Menon RS. 2001. Neural Correlates of Traumatic Memories in Posttraumatic Stress Disorder: A Functional MRI Investigation. Am J Psychiatry 158: 1920-1922.) This certainly raises the question whether such thalamic acivation due to bilateral stimulation contributes to treatment effect. Finally, it has been drawn to my attention that the recent meta-analysis by Davidson et al. that supports the notion that bilateral stimulation does not produce an effect shows in fact that bilateral stimulation may play a role if one looks at traumatized populations when compared to student analogue populations (I hope that the person who pointed this out to me will comment on this if I have inaccurately quoted them). **In addition, the one study that replaced installation trials with additional desensitization trials found no differences between the groups (Cusack & Spates, 1999). ** This finding is totally consistent with my own clinical experience with EMDR in that when traumatic memory processing is continued, the majority of clients will move into adpative material without cueing from the therapist. Furhtermore, it is consistent with PTSD treatment in general in that once traumatic material is resolved, adaptive functioning is increased. The big question that remains is whether there are differences in the processing of traumatic memories between EMDR and exposure. **While it certainly may be true that other procedural variations may eventually come to be shown to make a significant difference, the burden of proof falls on those saying that these procedures actually make a difference, not on those of us who question whether they make a difference.** EMDR is a fairly new procedure dating back to 1989, and the textbook being published in 1995. The first step was obviously to document its effectiveness. Whether the more controversial elements of the treatment such as the bilateral stimulation can be supported by empirical findings remains to be seen. **Regarding the comment about somatic sensations, I have to disagree. The manner in which somatic sensations are addressed in EMDR may be somewhat unique, but cognitive-behavior therapy does not ignore somatic sensations. Building on Peter Lang's research into visual imagery and his bioinformation theory, CBT techniques that utilize imagery (e.g., imaginal exposure therapy) frequently incorporate stimulus and response propositions, including the somatic sensations caused by emotional responding (e.g., feel your heart beating). In addition, the focus on somatic sensations is a very specific target in CBT for panic disorder, which uses a variety of exercises to actively evoke the somatic sensations of panic.** There is a crucial difference in EMDR that those somatic sensations are not necessarily attributed to emotional responding, as is often the case in CBT. While cognition, emotion and physical sensation seem to seemlessly interact in normal individuals, in traumatized individuals the physical sensation often is primary. EMDR specifically focusses on that physical sensation, asking the client to attend to it with mindfulness until it no longer reoccurs. Perhaps you are aware of studies that I have not yet seen. However, to the best of my knowledge there is not a single study of EMDR that has systematically varied the duration of imaginal exposure while keeping all other aspects of the treatment the same.** It probably is impossible to systematically vary length of exposure in EMDR, as this would violate the standard treatment protocol that essentially allows the client to free associate material. When one watches EMDR and CBT treatment tapes is is blatantly obvious that relatively little time is spent on the targetted traumatic event. Furhtermore, EMDR does not require exposure homework when used for PTSD. This has been addressed in the literature. To what extent the specific amount of time of actual exposure has been kept track of I am not sure at the moment. Maybe another reader can fill in here. At this point in time, to the best of my knowledge, there is no empirically validated treatment for Complex PTSD. When I refer to Complex PTSD and/or DESNOS, I am referring to a symptom constellation that involves significant dissociative symptoms and affect dysregulation. As previously stated, based on clinical impression, EMDR, while still providing a signifcant treatment challenge, seems more tolerable than Exposure. Yes, this remains to be empirically validated. Anxiety and fear appear to have differerent effects on pain perception where fear reduces pain and anxiety enhances it. This raises the question about endogenous opiod involvement. Dissociation, for instance, appears to involve excessive opiate release (e.g. Bohus et al. 1999). The us of opioid antgonists seems to interfere with exposure treatment , but seems to enhance the effects of DBT (Bohus) and there are some preliminary findings that it increases the treatment effects of EMDR. The latter remains to be replicated in a double blind study.
****Further, in contrast to exposure therapy, there does not appear a dose dependant relationship between length of exposure and treatment effect.**
**Beyond your clinical experience, what data can you site that indicate exposure therapy is not effective with victims of multiple traumas?**
**I can't speak to differences between phobias and PTSD at the level of neurotransmitter release, as I don't know the literature in this area.**
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