EMDR FORUM ARCHIVE, 2000
Re: differential mechanism
Shawn Cahill · 10/31/01 at 10:33 PM ET
Ulrich: **One view is that it is just good therapy, amalgamating different effective ingredients of many different psychotherapies and sharing many aspects with exposure therapy. Exposure therapy in contrast to EMDR is well grounded in behaviour therapy, one of the major theoretical approaches within clinical psychology - albeit it should be pointed out that it remains a theory and an active mechanism has thus far not been identified.** One can certainly argue that contemporary CBT theory is "just a theory," but let's not lose sight of the fact that it has developed out of a substantial body of research. CBT theory certainly has much more support for its propositions than psychoanalysis or thought-field-therapy or, I would venture to say, than Shapiro's Accelerated Information Processing model. Although it is true that, ultimately, all current theories are probably wrong, it is not true that all theories are equal. **There are also some clear differences between EMDR and exposure, as well as other psychotherapies. The major one, apart from the controversial bilateral stimulation, is that EMDR includes a specific focus on somatic sensations and the body that does not exist in other psychotherapies.** The observation that there are procedural differences between EMDR and other forms of therapy does not, in and of itself, mean that these differences influence outcome or that different/additional mechanisms of action are involved. Systematic desensitization and imaginal flooding are quite different therapies, procedurally speaking. However, years of dismantling research failed to support Wolpe's notion of recipricol inhibition and instead found that the effective element of systematic desensitization was repeated exposure to fear-related images, the same primary ingredient in imaginal flooding. Subsequent research went on to show that in vivo exposure was even more effective than imaginal exposure. Again, however, there is no basis for inferring the in vivo exposure involves different processes than imaginal exposure. 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). 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. In addition, the one study that replaced installation trials with additional desensitization trials found no differences between the groups (Cusack & Spates, 1999). 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. 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. However, whether some component of therapy is unique to EMDR or common to other therapies, the burden of proof is on proponents of the methodology/therapy (whatever methodology is under consideration) to show that the feature contributes to outcome. At present there is no evidence that the somatic focus in EMDR contributes to treatment efficacy. To provide a balanced discussion, the evidence for a specific role of interoceptive exposure in CBT for panic is still limited, although researchers are attempting to address this issue. Theoretically, we think that interoceptive exposure improves outcome beyond that of in vivo exposure, plus cognitive restructuring, plus breathing retraining. Empirically, however, I'd say the research is not yet as convincing as it could be. **Further, in contrast to exposure therapy, there does not appear a dose dependant relationship between length of exposure and treatment effect.** 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. Until this study has been done, there is no basis for claiming that there is no dose-dependent relationship between length of exposure and treatment outcome. Indeed, if there were no relationship whatsoever, then zero exposure would be adequate, which is unlikely to be the case. **From a clinical point of view that is corroborated by my own experience with both exposure and EMDR treatment, the lack of effectiveness of exposure with multiple traumata, specifically Complex PTSD stands out. While EMDR treatment of Complex PTSD is difficult at best, often requiring lengthy treatment, positive outcomes nevertheless seem much more likely. Clearly, this impression needs to be supported by empirical findings.** Beyond your clinical experience, what data can you site that indicate exposure therapy is not effective with victims of multiple traumas? The first two studies showing the efficacy of exposure therapy were conducted with Vietnam veterans, presumably a multi-trauma group (Keane et al., 1989, Cooper & Clum, 1989). The efficacy of CBT (exposure plus cognitive restructuring) among veterans was recently replicated by Glynn et al. (2000). A study conducted in Spain conducted sub-group analyses based on whether their female subjects were adult assault victims or victims of CSA, which typically involves repeated instances of abuse. CBT (combination of exposure, anxiety management, and cognitive therapy) was equally effective (Echiburua et al., 1997) in both populations. Epidemiological studies tell us that prior trauma is a risk factor for subsequent trauma. It is statistically likely that extant studies of treatments for PTSD are likely to include a good number of individuals who have experienced multiple traumas. Thus, the subject samples in the various studies of PTSD may not be as rarified as some have suggested. However, we are in agreement that further research should decide this issue, and not attempts at persuasive communication. **Further support for a potentially different mechanism comes from treatment response of phobias to EMDR. EMDR, in contrast to PTSD, where it is effective as a stand alone treatment, is not effective alone in phobias. This is taken into account by the so-called phobia protocol that requires the therapist to contract with the client to engage in a exposure exercise (though quite time-limited) once EMDR processing has been completed. This supports the notion that exposure and EMDR can be additive in effect but that they may have a differential underlying mechanism.** Again, I have to disagree. The arguments about level of treatment fidelity in the studies of EMDR for phobia not withstanding, the pattern of results in the EMDR vs. participant modeling studies is quite understandable in terms of the common procedural element of exposure. There is considerable evidence that imaginal exposure alone is somewhat helpful, but that in vivo exposure is by far superior. It is quite possible that in vivo exposure is more effective because it does a better job of activating the fear network than does imagery. In vivo exposure may do a better job of providing disconfirming evidence. For example, having the experience of touching a real snake and not being bitten is much more credible a source of information than imagining touching a snake. However, the difference is one of degree, not kind. Imaginal and in vivo exposure may work through the same mechanisms, with in vivo simply being more effective in recruiting those mechanisms. **I suspect that this difference is attributable to differential neurotransmitter release secondary anxiety and fear, as well as due to dissociation being a significant aspect of PTSD but not usually of phobias.** 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. Also, I can't speak to any differences in psychological treatments in altering neurotransmitters. Are there any data to show specificity between different psychological treatments for different anxiety conditions on different neurotransmitter systems?
I take your opening line as an invitation to participate further in this forum. You raise several issues. I have reproduced your comments within a series of asterisks, followed by my comments.
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