Thursday, July 27, 2006

IFA conference Day 1 and 2

I am currently in Dublin attending the IFA conference. Here are some interesting talks I have been to.

Gerald Maguire was talking about drug treatment. He also discussed the Pagoclone results. However, he did not reveal much more than at the press release on the Indevus website: see my earlier posts. He said that the journal that they submitted the results to has an embargo until their own press release. And this has not happened yet. Apparently, it is a journal that both practioners and medical doctors might read. So I guess they are aiming for Nature, Science, or Lancet. I asked him whether they take care of the possibility that a few severe stutterers significant improvements can distort the data. He said that they take very severe and mild stutterer out before the stats. To summarise, we need to wait a bit more for more meat on the study. However, he did reveal a bit more on the open-label extension. 90% of the participants kept on taking Pagoclone after the trials. He argued that this is promising.

Katrin Neumann spoke about her group's brain imaging studies on un-assisted recovered stutterers, and compared them to stuttering people and after-therapy people. I cannot remember the details now. But effectively un-assisted recovered stutterers and after-therapy stutterers show differences. She said that a region called BA47 (I think) is activated in un-assissted recovered stutterers. This region seems to have taken over some compensation that made this people fluent speakers. But people who underwent therapy showed different activations. Sorry, I am not being very clear. Just too many slides for 30 minutes.

Per Alm gave a talk on his pet theory that the basal ganglia is crucially involved in stuttering which leads to him explaining many stuttering facts (like fluency enhancing tasks) with the medial and lateral pathways for automatic speech and more-foccused speech. I spoke about this before on this blog. But it was good to hear it again.

More later. I need to go now and prepare my talk for tomorrow!!

Thursday, July 20, 2006

IFA conference: RCTs

I have just started writing the article for my upcoming IFA presentation: "Lies, damned lies, and random control trials". The title might be a bit strong, but in today's world you need to get out strong message to get people's attention! The presentation is about the use of random control trials (RCTs) in stuttering. In the last year, two main treatment studies have used RCTs: the Pagoclone and the Lidcombe study. I want to show that RCTs cannot just be blindly applied to study the efficacy of treatment studies. This is especially the case for early-childhood dysfluencies.

Here is what I say. This is typically the result of months long subconscious brain storming and discussions with others.

First, I will explain what an RCT is. I have to admit that I have never been formally trained to know what an RCT is, so I have to make it up and looking at a few sources. What I understand as the standard form of RCT is the following: You have a group of people affected by a condition (high blood pressure, AIDS, worm infection, etc). You have a medication which you administer in form of a pill, and you want to see whether the treatment is effective. You split the group into two subgroups: a control group, and the treatment group. You have to do this in such a way as to create the same type of group; for example you select them randomly, and possibly control for the age or gender in each group. You give a pill to both groups, but only the treatment group receives the true medication and the control group a non-effective substance. The level of the condition is measured in both group before and after the test phase.

... I need to drive to the airport now .... still havent written the talk... i'll do it on my laptop... I will fly to Estonia first visiting a friend and doing a day visit to Russia! Then I am going to Dublin for IFA.

Sunday, July 16, 2006

Abstracts from Nijmengen Conference

The abstracts of the 2006 Nijmengen conference is out: look on their website under Abstracts, and you will get a pdf file. Thx to Oren for this information! The conference is by far the most scientific one that also deals with stuttering.

Thursday, July 13, 2006

Working on my IFA contributions

I am currently working on my contributions to the IFA proceedings. The deadline is on Friday, but sending it by Monday morning if enough. Unfortunately, I haven't started with the articles nor the presentations yet! And rumors go that others haven't done much more either. This is a typical occurrence for conferences. In many cases, deadlines are postponed by a week or two, and I would be surprised if the same happens here.

So what am I going to talk about? The first talk is rather low-key and non-controversial. I am going to give a workshop with "How should we use the Internet to help researchers and do meta-analysis?". I am hoping that people are discussing ways to utilise the Internet for research on stuttering. As a warm-up, I will give a quick presentation on different ways on how this could be done, and on what the obstacles are in my opinion. And then hopefully the participants will "take over" and a lively discussion will start. Here is a list of Internet utilities that I find useful:

- Pub Medline: Internet archive of all published articles on stuttering
- Messenger and VoIP: Chatting and talking to other researchers for free (I have done this extensively with Per Alm, Roland Pauli, and Oren Civier)
- Email: goes much faster than writing letters. Yaruss & Onslow debate (but this one is old by now! :-)
- Pdf / Word Files: you can easily send your research article to someone. (I often ask researcher to send me their article).
- Mailing List:
- List Archive: like Judy Kuster
- Blog: THE STUTTERING BRAIN of course, always the latest on stuttering (big readership after Pagaclone story broke=
- Replis in Blogs: Ingham.
- Online conferences:
- Wikipedia entry
- Open articles & Replies:

Some issues:

- researchers have no time.
- too many sources.
- secrecy dominates.
- old generation.
- no real scientific debate: more teaching of others
- too much information.
- difficult to judge quality of information
- etc

So I will make 4-5 slides for this workshop, and write 1-2 pages. That's it. The other article will be hard-core science. I want to make people aware that you cannot just apply the standard random control trials framework for stuttering. I have done a few statistical simulations, and show that for example the Lidcombe results are not as clear as they think.

More tomorrow.

Tuesday, July 11, 2006

Travel companion(s) after IFA?

I will be at the IFA conference in Dublin in two weeks' time.

The conference ends on Friday midday, I think. My flight goes back on Monday evening from Dublin. So I have from Friday midday to Monday evening to travel around Ireland. But I havent planned anything yet. I might rent a car.

If you are also at IFA and have some extra days, pls let me know and we can join forces! Preferences are obviously given to girls, people at my age (or younger :-), and stutterers! :-)

My email is tom DOT weidig AT physics DOT org

Monday, July 10, 2006

Auditory system: cause or necessary condition only?

I have spoken about the findings of several research articles that claim an abnormality (in activation or anatomy) in the auditory system, and its consequences: see here. I said that it dont believe that "bad hearing" is causing stuttering.

While cycling up a long hill (trying to imitate the Tour de France), I suddenly came up with a way that might explain lower activation in auditory regions. Here is the line of arguments:
1) People with PDS at birth have no different hearing capabilities (or potential for) than the average population.
2) Learning to speak effectively involves fine-tuning your neural networks to produce speech, and this is only possible with feedback from your auditory system. You need to hear to be able to fine-tune your speaking networks. That's why deaf kids cannot learn to speak properly (except if they get a Cochlane implant).
3) Some kids have a better auditory system than others, but they all manage to learn to speak.
4) Now, I assume that dysfluent kids have an inherent weakness / abnormality (genetics or neurological incident), and the fine-tuning becomes more difficult.
5) Only the kids that have abnormally good hearing are able to do the fine-tuning and recover. The kids with average and lower activation do not, even though had they not had the weakness / abnormality they would have.
6) So looking at dysfluent kids you will find average hearing capabilities (thinking everything is fine). But in adults with PDS you will see an on average lower activation of auditory system.
7) One can even argue that only a temporary delay in the development of the auditory system around age 3-5 will hinder fine-tuning. So you wont see a statistical signal either for all dysfluent kids or for stuttering kids after age 5.

This is only brainstorming. But this scenario shows well that something might not be a cause of stuttering (the weakness / abnormality is), but a necessary condition for it to happen.

Tuesday, July 04, 2006

Timeline of remission?

I am looking for the time line of remission (i.e. the recovery from (early childhood) stuttering).

About 5% of all children have disfluencies, but only 1% develop persistent developmental stuttering (PDS). I am interessed in how fast the 5% go to the 1% baseline of adulthood. Is it within 1-2 years of stuttering? So after the age of 5 or 7, 80% have recovered.

I am especially interested in the age group 9-13. Can one study therapy effect like in adults, or is there still a natural recovery rate to consider.

If you know of any literature, please let me know.

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.