Sunday, July 02, 2006

Yaruss - Onslow (Part II)

the second part of their debate...

Regarding future application of theory, you imply that history must repeat itself, whereas I only say that it might. To prevent this, we both highlighted safe-guards, such as that the theory must generate testable hypotheses. Meanwhile, it is true that the data for other treatments are presently lacking–much work remains to be done. To accomplish this, I would like to have, as a starting point, a framework to support that therapy and the necessarily data collection.

Uni-dimensional explanations do not provide an appropriate starting point, for stuttering encompasses more than just speech disruptions, and the factors involved in the onset and development of stuttering involve more than just speech disruptions. Thus, I would challenge your claim that “multifactorial theories of stuttering are completely and irretrievably wrong.” It might help if we were to differentiate between multifactorial theories and resultant (or non-resultant) treatments. Obviously, theories cannot be used to treat stuttering, but they can provide the basis for a testable treatment.

As we move toward collecting the necessary data, we might benefit from starting with a well-constructed theory that provides an explanation of why we might manipulate certain variables. That would then lead to studies, ultimately including clinical trials, that demonstrate the validity and efficacy of a treatment program. Lidcombe has accomplished this goal from an atheoretical perspective, if I read you correctly. I believe the same goal could be accomplished (though this has not yet been the case) from a theory-driven perspective.

Yes, a new theory can lead to a new treatment checked by clinical trials. But not through a multifactorial theory.

There is nothing wrong with multifactoriality. Life is multifactorial, so is love, a toothbrush, and so is stuttering. However, arguing that because stuttering is multifactorial, therefore the cause of stuttering must also be multifactorial is an error of logic. This logical fallacy is called the representativeness reasoning: to believe that the nature of effects reflect the nature of causes (see Onslow, Attanasio, & Packman, 1998).

Additionally, multifactorial theories do not do what a theory should do: explain things (Packman & Attanasio, 2004). Why do word and syllable repetitions predominate at the onset of stuttering? Why can stuttering be intractable for a lifetime? Why do those who stutter have problems with tapping finger sequences? And why do those who stutter have the problem while playing wind instruments?

I found the list of factors you find relevant to the explanation of stuttering to be enlightening. In developing a theory to explain the phenomena of stuttering, it is appropriate to begin by listing those phenomena. Here are some questions that strike me: Why does stuttering start at a time of rapid expansion in linguistic, motoric, and temperamental aspects of children’s development? Why do people who stutter react to their stuttering in the way they do? Why does the occurrence of stuttering seem to be so closely linked with aspects of language planning in both children and adults? Specifically, why is stuttering not distributed randomly with respect to linguistic, situational, and experiential variables? Why do people who stutter show differences in motoric stability and linguistic processing, even when they are not engaged in speaking tasks? What about differences in neural function and possibly even structure? And temperamental differences? Finally, why do multiple loci seem to be implicated in genetic modeling?

This is not an exhaustive list...just a start of the questions that would need to be answered by any comprehensive theory. Posing a single factor to explain all of this would seem unlikely. Posing multiple, interacting factors gives the opportunity to save more of the phenomena.

Moving back to treatment, I would like to see further discussion of what might be going on for children who do not recover through Lidcombe, and what might be changing in children who do recover through other therapies. This would enhance our understanding of the disorder from both a theoretical and clinical perspective, and it would provide better justification for why we do what we do in therapy. Until we understand the reason for the change in fluency to supplement the basic fact of the change itself, I will remain dissatisfied with the knowledge base and will seek to identify some means of explaining the many and varied phenomena of this disorder.

Clinical trials and cohort studies give me no reason to think that there is a group of children who do not respond to the Lidcombe Program. Jones et al. (2000) reported 261 treated children of which 250 completed Stage 1. Thus, 250 children attained zero or near-zero stuttering. The remaining 11 did not complete for reasons common in speech pathology treatments, such as moving away, illness, severe family problems. These findings were replicated by Kingston et al. (2003). A similar picture has emerged with the Phase I, II, and III clinical trials that have been published.

Still, questions remain about its real-world effectiveness, for not everyone may administer the program as efficiently or as effectively as you and your colleagues appear to. We have discussed non-responders more than once before. You may not see them in your studies, but I know of other clinicians who see them in their daily practice. Clinicians have consulted with your team and other Lidcombe practitioners, and your team is quite responsive in trying to help clinicians in such cases. So such cases seem to exist.

As for other treatments, in a preliminary study of the approach used at our Stuttering Center (Yaruss et al., in press), we found that 17 out of 17 children enrolled in the program (not just those treated to completion), achieved improved fluency and maintained it over a follow-up period of at least 2 to 3 years. Most required only the 6 sessions that the program is designed around, but a few children required more treatment. Why did the 4 children require more than 10 sessions? Ultimately, these children also recovered, but the lack of immediate success might teach us about the disorder. So, we look at factors like language skills, motor skills, temperament, family history, and life experiences to help us better understand the treatment and the disorder itself. Have you conducted similar inquiries with Lidcombe? What theoretical framework did you use?

Again, there is no scientific evidence for the existence of a substantial cohort of non-responders. Also, my position is that the population effectiveness of the Lidcombe Program is currently unknown to science, because no effectiveness research has been conducted. But we have evidence for its efficacy. Epidemiological studies would be needed to address the capacity of the Lidcombe Program to impact at the clinical population coalface. We have put in place various ways to facilitate that effectiveness. For example, a Lidcombe Program Trainers Consortium has been established in seven countries ("Lidcombe Program Trainers Consortium Grows in Europe," 2005). Each year, hundreds of clinicians around the world receive training from Consortium clinicians who meet published scientific benchmarks for the treatment.

If you know of someone who consistently does not get children to stop stuttering with the Lidcombe Program, there are at least two possible reasons. First, they may have not done the treatment according to the manual that can be downloaded from our website. Second, they may benefit from Consortium training in the treatment.

You accept that the LP has the best clinical trials efficacy research. So, what treatment do you select for a four-year-old stuttering child in need of treatment?

I treat as described in Yaruss et al. (in press), but I also work to validate that treatment and collect data to refine and improve the treatment. Though I do not use Lidcombe, my staff has received training and we have discussed the principles of the treatment in detail. Furthermore, I always encourage clinicians to participate in the consortium training directly if they are considering using the Lidcombe program. I fear that many might not be using the treatment correctly, and without an understanding of why the treatment should work, it is impossible to know what the results from various modifications might be. This is yet another reason I keep returning to the value of theory, and why I asked the question that started this dialogue.

For my part, before I accept a treatment such as Lidcombe, I want to have a better idea about the nature of the changes that are taking place. Thus, in my clinic, we are actively engaged in examining not only the efficacy of the treatment we use, but also the mechanisms behind the observed changes. Much more work remains to be done, but our work, and that of others, is progressing.

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