Sunday, May 15, 2005

I'll pay Dave Rowley a drink at ODC!

Thx Dave for writing the first comment on my blog!!! Despite me misspelling his name, linking him to his official rather than personal website, and the Comment section at www.blogger.com being a bit cumbersome. I will be forever grateful! ;-)

The way that the blog site handles comments is indeed a bit cumbersome. You can get to the COMMENTS page by clicking on the x Comments at the end of my posts. Each post has a comments page to it. On this page, you can read the comments or write one yourself, or reply to another comments.

I'll see if I can make the layout more intuitive by using another template or edit the code myself. I just need to take some time to understand the HTML add-ons that they use.

Concerning Dave's question "Do you think there are any brain changes before and after!?". My answer is: It depends on what you mean by "brain changes". I can think of three meanings: 1) an un-detectable change in the brain (like new memories, learned behaviour) 2) a detectable functional change in the brain (like a region is now under or overactivated in comparison with the activation for the same task before), or 3) a detectable structural change in the brain (like the auditory processing region in a blind person becomes larger).

It is clear that the/any therapy leads to type-1 changes, as most patients are noticeably more fluent just after intensive fluency shaping therapy , for example. There must be something different to their brains. On the other hand, relapse is the norm, and thus this change is not very long-lasting.

Concerning type-2, I know of two brain imaging studies by Neumann et al. and by de Nil et al. that see that the typically PDS right-brain activation disappears about treatment (therapy), and more. So, the answer is yes there are detectable differences in the brain, assuming their results are OK. But I think the point might be that the activation has changed because the brain calls up a different software, but the old one leading to stuttering is still there waiting...

Concerning type-3, there is not evidence. I guess this is possible, but only over the long time. To which degree is not clear to me?

More research is needed.

Interesting questions from the top of my head: Does this change also happen for post-block modification or drugs? What is the role of the PDS severity? How much can the brain really change? Can you do brain scans and predict whether a person is more likely to get better? Can you distinguish in brain scans between neurological cause and the habits/learned behaviour? I.e. two people might stutter equally strong, but one has 10% neurological 90% habits and the other 90% neurological and 10% habits? Making therapy more individual might decrease relapse?

In my next post, I will talk about computers/software in therapy.

Tom

1 comment:

Roger Ingham said...

Dear Tom:

I want to put on your blog site some of the comments we’ve had recently by email. This might be a bit cumbersome, but let’s see if it works.

First, I want to tell you, for what it's worth, that I am enjoying your blog page writings more than I have enjoyed any other web page material of this type. Your account of your elucidation of our work and the scientist-practioner clash was lucid and thought provoking. Let me comment on a couple of items.

Second, regarding your comments concerning stuttering measurement. You had indicated that “correlation between the regions and the frequency of stuttering is important, but it does not say anything about casual links, which is needed to distinguish between cause and effect. Auditory regions and cerebellum seem to be effects: they are physically far away and minor branches of the normal speech process flow.” My response is that I honestly don't know how we determine the effects of anatomic proximity in the brain, but there is no doubt that temporal lobe region is intimately associated with speech production.

Third, you expresses some concern about the significance of the findings concerining neural region overactivations. As you pointed out “Did not Katrin and Christine Preibisch find that in people with PDS who stutter midly the right frontal operculum is more activated than in those who stutter more severely? And at some point I digged up an open surgery case in Harvard where when they stimulated the rfo, the person started stuttering.” My response is that the Neumann et al findings are a bit of a puzzle. I think, though, that we have to balance them against replicated findings that tend to differ from their RFO results.

Fourth, you suggested that perhaps “one way of dealing with effect/cause is to knock out a region with TMS. But I am not sure whether this can be done precisely enough.” In reply I pointed out that is the main focus of our work in San Antonio at the moment. We have invested a huge amount of time and money into refining the TMS aiming system. And by the end of the summer I think we'll be in good shape to start exploring some of the options. We are currently running some preliminary experiments on ourselves. So far, so good.

Fifth, you indicated that "there has been no constructive approach to developing better therapies." I would have to disagree. There has been a very constructive approach adopted by some of us in this domain. The work behind the development of therapy for children and our own work on refining the parameters of prolonged speech and then converting them to therapy has certainly not been a hit and miss affair.

Anyhow, just to reiterate, I am very much enjoying your observations.

Roger Ingham