EMDR FORUM ARCHIVE, 2000
Re: differential mechanism/ SUDS/ eye movements
Cahill · 11/10/01 at 9:50 PM ET
Hi Louise, I'm glad you've enjoyed reading the exchange thus far, and welcome to the fracas. Your comments may, at some point, lead me down the road of "distraction" which I had attempted to avoid in my earlier exchange with Susan. Not yet, but maybe later. In the mean time, I wanted to post a few brief reactions to your comments. If I understand your point, the observation that SUDs is sensitive to change in EMDR even when change is not detected on outcome measures suggests the operation of a different mechanism than is present in standard exposure. And you hold this to be the case regardless of whether or SUDs reduction in therapy is related to outcome. Perhaps I'm splitting hairs here, but I can agree with you only so far. Here is where we agree: The pattern you describe does suggest the possibility of some mechanism operating in standard (i.e., eye movement) EMDR that is responsible for within session fear reduction that is not present in a no-eye movement variation of EMDR (e.g., Boudewyns et al., 1993) or in standard exposure therapy (Rogers et al., 1999). Now where we may be in disagreement is whether or not treatment outcome is mediated through the same mechanism as standard exposure therapy, this new mechanism responsible for within-session fear reduction, or some other mechanism. Unless it can be shown that there is a relationship between fear reduction in session brought about by eye movements and treatment outcome, or until some other procedure unique to EMDR is shown to significantly associated with outcome, then I suggest that the parsimonious answer is that treatment outcome is mediated by the same mechanisms acting in exposure therapy. Now, as to what this new "add-on" mechanism may be, you offer two competing theories that have developed out of analogue research. The Andrade/Kavanaugh hypothesis that eye movements reduce image vividness, leading to reduced affect and the van den Hout's hypothesis that eye movements reduce affect intensity which then leads to decreased vividness. If I had to go with one or the other of these hypotheses, I'd more inclined towards the Andrade/Kavanaugh hypothesis. Malloy and Levis conducted a study of imaginal exposure with students who were mildly snake phobic in which they measured SUDs and image intensity over the course of several repetitions of a fear relevant scene. In addition, they manipulated the number of stimulus modalities included in the imagery (sight only; sight and tactile stimulation; sight, tactile stimulation, and pain cues). Not surprisingly, the greater the number of stimulus modalities included in the imagery instructions, the greater the level of self-reported fear. Also not surprisingly, fear declined over successive trials. Of interest to our discussion, image clarity or vividness increased even as anxiety decreased. The interpretation they offered was that low image vividness was an avoidance response. As fear of the image extinguished, the motivation to avoid the image was reduced and, accordingly, there was an increase in image clarity. While an appealing interpretation, the study was not able to control for simple effects of practice on image clarity: Maybe their imagery got better because of practice and the relationship with fear reduction just an accidental correlation. All that said, I'm still not firmly convinced the effect of eye movements is a substantial effect in explaining the efficacy of EMDR. First, there are two few relevant observations with the full clinical procedure. Additional studies should pay attention to this issue. Second, if the Andrade/Kavanaugh hypothesis is correct and, as I understand their results, other forms of bilateral stimuli such as tapping are not as effective as eye movements. This of course makes sense in that non-visual/spatial motor tasks will not interfere with visual tasks (imagery) as much as a competing task that involves the visual system (e.g., eye movements). Yet in terms of outcome, EMDR without eye movements is just as good, whereas if the Andrade/Kavanaugh mechanism would predict that eye movements should produce better outcome. Also, we should keep in mind several analogue studies that did not find eye movements to reduce SUDs more than comparison groups (e.g., Tallis & Smith, 1994; Merckelbach et all, 1994; Haw & Dickerson, 1998). Your interpretation of how the Andrade/Kavanaugh mechanism may play itself out, if I'm understanding you correctly, boils down to one of titrating stimulus exposure. In other words, it allows patients to experience the image in a less intense form. Presumably, this reduces avoidance of image and thereby promotes processing. This sounds a lot like the Malloy and Levis hypothesis. However, if the only thing that eye movements are adding to treatment is titrating the level of exposure there are a couple of issues that may be raised. 1. Is this the only way to titrate the memory? If not, is this the best way to do so? Within the Foa model of exposure, titration of the memory is done in a variety of ways: having the person engage in the exposure with eyes open, having them tell the story in the past tense (rather than the present tense), having them write the memory rather than imagining it, breaking the memory into chunks and starting with the less intense pieces first, starting with a general telling of the story and working up to more and more specific details. The point here is that there are probably a lot of ways to titrate the memory in addition to disrupting the visual-spatial sketch pad with eye movements. Also, titrating the memory should be seen for what it is, an application of the concept of a hierarchy that has long been part of exposure therapy. 2. If you believe the actual mechanism of eye movements is to titrate the memory, shouldn't this be the explanation you offer your patients, rather than the standard EMDR explanation that it somehow physiologically triggers the adaptive processing mechanism? It seems disingenuous to believe the procedure works through one mechanism while telling the patient it works through a different mechanism. Also, again if the point is titration, then why not offer the patient a range of choices rather than imposing eye movements as the first tier and only going to others if problems with the eye movements arise? Finally, perhaps you can answer a question I posed to Ulrich (the second of two posts each called Part 6, mislabeled by accident): What is the difference between this dual attention mechanism hypothesized by the Andrade and Kavanaugh group and the older notion of distraction? Is there any THEORETICAL reason to think that a dual task would enhance memory processing rather than detract from it? As I noted earlier, if symptoms persist because the memory has not been adequately processed, and processing requires cognitive resources, how is it that dividing these cognitive resources between two tasks leads to better processing? Thanks for your participation in this discussion. Also, the Kavanaugh et al. (2001) and van den Hout (2001) studies are new to me. Could you provide the full citation? Thanks.
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