Monday, April 30, 2007

CNN talks about stuttering


GUPTA: Jerry Maguire grew up to be Dr. Maguire.
MAGUIRE:I likely stuttered the rest of my life.

Sunday, April 29, 2007

Dysfunctional stop signalling??



And a more empirical argument.


No shared environmental influence!!!!

At last, I can report of an interesting piece of research. The authors Dworzynski, Remington, Rijsdijk, Howell, and Plomin have used data on 1000s of twins to study genetic relationships in recovered and persistent stuttering: see Am J Speech Lang Pathol. 2007 May;16(2):169-78 or here. Remember twins can be monozygotic (the same DNA), or dizygotic (share roughly half the DNA like siblings do). If the monozygotic twins share a disorder more often than dyzygotic twins at statistical significance, then the disorder is genetic because the only difference between them are the fact that they share either all the genes or roughly half the genes. Though the interesting aspect about twin studies is that you keep the environment relatively fixed, i.e. twin grow up in the same environment. A second advantage is that technically speaking this is simple statistical computation, that even non-quantitative researchers should not be able to mess up. There are surely negatives but I am not sure, probably the inability to locate genes.

Building up a twin pool is hard work but very lucrative scientifically speaking and ensures divine reverence by other scientists. Every research field undertakes a pilgrimage to these pools, and after worshipping the holders of the holy pool are allowed access to study the genetic influence.

They found that
Stuttering appears to be a disorder that has high heritability and little shared environment effect in early childhood and for recovered and persistent groups of children, by age 7.

Monday, April 23, 2007

Briefer on basal ganglia

Here is a description of the basel ganglia that Rafael sent to me. Actually, it's from Per Alm and published in the proceedings for the IFA conference in Dublin 2006.

The basal ganglia circuits are organized in a direct and an indirect pathway. These two pathways are assumed to work in synergy to modulate the activity of the frontal cortex: the indirect pathway providing a diffuse inhibition of cortical activity and the direct pathway providing focused activation of the desired action. Furthermore, the two pathways are dominated by different types of dopamine receptors, D1 vs. D2, resulting in differential effects of dopamine. The cueing functions of the basal ganglia to the SMA are dependent on a clear distinction between focal activation and the surround inhibition of the cortex, in other words, a good signal-to-noise ratio. Based on this model it is easy to imagine that the cueing of the basal ganglia can be distorted in different ways. Too weak focal activation of the direct pathway would result in deficient activation of the desired action, for example difficulties in initiating speech movements. On the other hand, impaired diffuse inhibition of the cortex, provided by the indirect pathway, could result in a combination of release of unintended movements and impaired release of the intended movement. These scenarios have clear parallels with the symptoms of stuttering. Basal ganglia motor disorders are characterized by motor initiation problems, involuntary movements, and deregulated muscular tension, often with co-contraction of antagonistic muscles.

Thursday, April 19, 2007

Do we fail to stop rather than to go?

Several researchers describe stuttering as the failure to properly initiate a sound. They also talk about the disturbance in the go signal. Today, I read a very interesting article by Vanderbilt psychologists Boucher, Palmeri, Logan and Schall about how the brain decides when to start or stop movements. The graph above shows the activation of the start and stop neurons; the task is pressing a button when green and stop when red. There are really two processes in the brain battling for supremacy!

Here is the essence of the article:
"We think of people who are impulsive as acting too quickly," Logan said. "Kids with ADHD are actually slower on the 'go' task than the control kids. It's not that they go too quickly; they stop too slowly."
Take this concept to stuttering, and maybe people who stutter are actually OK on giving the go signal, but are BAD AT GIVING THE STOP SIGNAL TO THE PREVIOUS SOUND. So a block is not actually the failure to have a go signal, but a failure to initiate a stop signal to the previous sound. It is worth pointing out that every human often corrects sounds that are ready to say, but may be we cannot actually send the stop signal to this sound and therefore disturb the go signal for the next sound.

Tuesday, April 17, 2007

The 60-million dollar gamble!




Does ADHD make it harder to become more fluent?

Lynne wrote an interesting comment:
My teen son has been diagnosed with ADHD-inattentive type and has stuttered since age 2 or 3. I have always felt that the two were tied together. He has a hard time using the techniques, and if he does, it's hard to concentrate on anything. Processing speed in class is much slower than what is expected and makes the task and speech worse if he is made to hurry.--Lynne
There are some researchers like Per Alm who see a link between the two. Lynne's son might have had some mild neurological incident around age 2-3 and therefore develop stuttering and ADHD-like symptoms. However, it might also be a pure coincidence. For example, some kids stutter and have asthma. That does not necessarily mean that both are related to each other. The kid might just have been unlucky to get both.

Nothing special here. But Lynne's observation is intriguing: ADHD-like symptoms seem to make applying speech techniques much more difficult. Based of this assumption, I can formulate the following prediction. Let's assume you have two possible casual sources of childhood dysfluencies: genetic (design flaw) and neurological incident (design implementation flaw). Kids with either or both of them start stuttering. Their brain tries to compensate to produce fluent speech. The kids with neurological incident are more likely to have ADHA-like symptoms, and are LESS ABLE to compensate. They are therefore LESS LIKELY to recover.

So I would predict that the share of stuttering kids with bad genes as opposed to neuro incident should DECREASE over time!!!

Tuesday, April 10, 2007

Looking to share room at ISA2007



Wednesday, April 04, 2007

Tom's oracle

Being dysfluent does not seem to be the only dysfunction we have. I have spoken about sub-standard dual tasks performance before. People who stutter are not good at learning or doing dual tasks (the details are a bit more subtle). Professor Webster from Canada was the first to study this experimentally; an excellent piece of science in the midst of the common appallingy low quality and headless research in stuttering.

Why should we be worse in some dual tasks???


We need to find out why. If we succeed, we will understand stuttering much better. And no-one can claim to understand stuttering if they cannot explain this effect.

This line of research is the key to the stuttering mystery, and a feast for a scientist:
1. it is not about speech. (but stuttering is supposed to be a speech disorder!)
2. it is a reproducable effect. (try to reproduce the same stuttering!)
3. it is a measurable and quantifiable effect. (try to quantise stuttering severity properly!)
4. it is free of psycho and behavioural noise. (try to disentangle how much of stuttering severity is bad habit, how much situational and how much fundamental!)