On brain research

I got an email from George D asking me interesting questions on brain imaging, which might also interest you.

George: It seems to me that there have been a few problems with the approach to the research. 1) All of the studies have been done on adult stutterers, and this will always leave open the question of whether the observed differences reflect acquired characteristics - or *learned* behaviours/strategies - or whether they really do reflect inherent, hard-wired neural differences.

The researchers look for across-the-sample CONSISTENT differences. This eliminates individual characteristics like "I use filler", "you have silent blocks". The pathways and activation would not be the same, and so eliminated.

Thus, individual coping strategies should be eliminated, but not systematic ones not e.g. everyone gets more tense. This makes things more difficult, but at the very least shows us what the core of stuttering is.

So what you see are correlations. The interpretation is of course more difficult, but by adding theoretical reasoning, including non-brain findings and varying experimental designs you can start to distinguish between what is a consequence and what a cause. This is currently underway.

George: Obviously, doing brain scans on little children (thus exposing them to radiation) is not ethical.

fMRI does not give out radiation, only a strong magnetic field. I think that researchers are now comfortable scanning younger children. But I dont know the details. Sounds like an interesting post for my blog! :-)

George: Most (if not all) brain imaging appears to have been done with fMRI or PET. PET and fMRI have inherently very limited temporal resolution, and to research stuttering, higher resolution is required because speech/language processing takes place in a matter of milliseconds. One idea is to use PET/fMRI together with magnetoencephalography (MEG), which has excellent temporal resolution. I guess this may already have been done??

Yes, there is a paper by Samelin. See here. But I am also surprised why so little MEG work has been done. I need to find out.

George: The number of imaging studies done on stutterers seems to be small, so the results may not be a true indication. Actually, I don't know whether the number of studies is small, but I suspect that it might be.

No, I have counted more than 10 studies. So it is pretty safe. In any case, it would be highly strange if brain imaging hadnt found any functional difference because our brain is sending the stuttering signal to our muscles. Structural abnormalities is another issue.

See here.

Myth propagation: Lidcombe

The stuttering research literature and its transition to the mainstream have always frustrated me. I hear people making statements based on research articles or some magical consensus view. However, the research rarely proves what people interpret from its findings, and its findings are often flawed due to weak methodology. And, the consensus view either does not really exist or is a good example of how the strength of an argument is not related to a majority supporting it (but you can argue that the likelihood of the statement being true is higher). Following up the lead of the source, and the source's source, and so on, decreases the certainty on who the source is and the accuracy of the interpretation of what the source actually said. As a teenager I spent my Christmas holidays in a youth winter camp in the Swiss Alps, and in the evenings we often played an interesting game, that I am sure most of you have played, too: You sit in a circle, and the first person whispers a message to the next person, and round it goes through the circle. The first person never got his first message back.

A recent example of my frustration is the random control trial research article on the Lidcombe treatment program for stuttering children. The mainstream talk is that this article has shown that the Lidcombe program effectively cures stuttering children. (Please note that I am not actually claiming that the authors say this.) I have spoken about the stats obsessively in several posts: see here. Today, I re-visited the article and actually realised that the interpretation possible are rather limited due to their design.

They have randomly chosen two groups of stuttering kids, and only treated one group. And they found that the treatment group is more fluent; and therefore claiming success. However, the standard random control trial setup has a different purpose: see whether there are above-placebo benefits. You administer a pill to BOTH groups, and therefore BOTH groups do not know whether they receive treatment or not. In the Lidcombe study, the treatment group and their parents knew that they received treatment. The extra fluency in the treatment group could mean three things:

1) Success due to the placebo effect: believing heals. (Admittedly, even placebo effect is good if it is permanent!)

2) Success due to additional-to-placebo effect: the Lidcombe study has a treatment component that is successful. This leaves open the possibility that all other known treatments like demand & capacity would be as successful. For example, the treatment component might be ANY extra attention given by parents to their stuttering child. A study by Franken et al. compared Lidcombe to demand & capacity and find no difference in outcome. (However, I think their sample size is rather small.)

3) Success due to unique-to-Lidcombe effect. Lidcombe is more successful than other treatment approaches because of treatment component X, Y, and Z.

As you can see the study leaves all three options open, but the mainstream talk is virtually exclusively about option 3 even though this is not the only possible interpretation of the data!!!!

More fluent without hearing

Sometimes I speak with Per Alm over Skype. I asked him whether people with PDS stutter less when they do not hear their voice. And he confirmed my suspicion. He also mentioned that van Ripper reports on two case studies where people with PDS became fluent after having become deaf. Of course, these are anecdotal findings.

And, we need to be careful not to read too much into this correlation between fluency and hearing. This type of findings does not imply that a bad hearing system is to blame for stuttering. I would rather guess that the person now needs to concentrate more on his speech, and this makes him more fluent. This would put the no-hearing-more-fluency findings into the category of fluency inducing tasks like singing, shouting, acting, speaking with a foreign accent, and more.

Stuttering after accident.

Here is a Mirror article on a UK singer Marc Almond who after a car accident started stuttering again. He stuttered as a child. Would be interesting to put him in a brain scanner!

PhD scholarship

Here is an advertisement for PhD scholarships, which could be linked to stuttering. Contact Robin Lickley, the younger Scottish generation's answer to Sean Connery. :-)

PhD positions funded by the European Commission under the Marie Curie Early Stage Research Training (EST) scheme are available on the Edinburgh Speech Science and Technology (EdSST) project. This is an interdisciplinary training programme in speech science and technology featuring a strong interaction between the two disciplines. Two of the available topics are applications relevant to stuttering:

Speech recognition applications for stuttered speech Dialogue training for people who stutter

Alternative topics which fit within the remit of EdSST are possible.

See http://www.cstr.ed.ac.uk/edsst/opportunities.html for further details.

Battle of the profs

They are still smiling, but soon they will be battling for truth: may the best win! The BSA magazine Speaking Out wants to run a debate between Scott Yaruss and Mark Onslow. Together with Speaking Out editor Andrew Harding, I will edit the debate for the BSA research committee. Should be interesting. I keep you updated and tell you when it's online. Most likely here where many past Speaking Out articles are. Thanks to the good work by Andrew Harding, and Allan Tyrer the BSA webmaster.

BSA Vacation Scholarship

Today is the deadline for the BSA Vacation Scholarship applications; I should have talked about the scheme a long time ago. :-( It is an initiative of the BSA research committee of which I am vice-chair and that I started in 2001 when I was a BSA trustee. We give students funding to do research work in stuttering over the summer to get them addicted to stuttering research. :-)

Read more here:

This year the Research Committee of the British Stammering Association is again running its Vacation Scholarship scheme to provide students with the opportunity to propose and execute a research project related to stammering. The project may take the form of original research or a review of existing research. Whichever approach is chosen the project should help the BSA to fulfil its vision of a world that understands stammering. Reviews should therefore also include a well developed proposal for future research for which the BSA could seek funding. The immediate aim of the scheme is to assist those who wish to conduct research into stammering, or related areas, in their future careers. The long-term aim is to increase awareness of the importance of research amongst professionals working with people wanting to improve their fluency.

Applications are invited from departments of speech language, psychology, medicine, social science or any allied disciplines, for students to work on a research project during the summer vacation. All applications should be submitted by the sponsoring departments on the students' behalf. Joint applications where two students share the work, and the bursary, are permissible.

Functional and structural abnormalities

Several research groups have now found functional and structural abnormalities in the brain of people with PDS.

Structural abnormalities:
Sommer et al
Jaenke et al
Watkins et al
Foundas et al

Functional abnormalities:
de Nil et al
Ingham et al
Fox et al
Neuman et al
Watkins et al
Salmelin et al
Mori et al
Blomgren et al
Stager et al

Lost student

I am a bit stressed. And no time for longer posts.

I recently chatted to a speech and language therapist, and she complained about the futile nature of studying for an exam on stuttering. What is the point of studying stuttering if everyone gives conflicting answers and not clear advice for treatment?

Are computers better?

I am wondering whether therapists can predict whether a child recovers or not more accurately than a simple computer algorithm... I could feed the algorithm with information on the age of onset, gender, and possibly family history, and then it would make a guess. I need to think about this more carefully.

Move your thumb

I heard that if you move your thumb while speaking, you stutter less! I am wondering that this effect has to do with the fact that the finger regions are close to the speech and language areas?

In a whim of a moment

Have you seen the recent movie Match Point directed by Woody Allan? Great movie: subtle and unpredictable yet realistic plot. The story plays in London featuring Upper Middle Class life, an ex-professional tennis player from a poor background climbs up the social ladder during his work as a tennis coach at the posh local tennis club. The theme is a common one: A small event can have a huge impact on your life. Remember the cliche: You miss the woman of your dreams by seconds. You get out of the bus seconds before the explosion. You miss the plane that crashes by seconds. And so on. I might have such a story, related to stuttering but not about my life.

In the neighbourhood next to my neighbourhood, a kid who stuttered lived. We never spoke but I knew he stuttered and I think he also knew that I stuttered interpreting from his facial expressions. During the summer holidays, the town council organised day summer camps, and he was there, too. One day I witnessed how he tried to explain something to a supervisor while we visited a mine museum. I thought to myself: My God, good lord I don't stutter that badly. Only later did I find out that I often stuttered as badly! You could sense that he really suffered also socially from his stuttering, more so than I did. At some point I lost sight of him. He was not at my high school, and then I left for England and the US to study and do a PhD.

Last year, I saw him again. He was also a spectator at the Open Beach Volley Ball tournament of my home town. (Over-)Loaded with years of self-help groups, therapies and involvement in the BSA and research, an evangelical fever came over me telling me: "You need to talk to him. Clear up your past. Ask him whether he also knew that you stuttered. And maybe give advise if he needs help." So I slowly approached him but then my courage disappeared. I felt a mental and stuttering block. He also looked a bit fearsome to me. He had gained quite a bit of weight, and really had a look of sufferance on his face. He looked uneasy with his life. So I told myself "leave him alone, you just shock him" and passed him, but we exchanged looks: he did recognise me, and might even have identified me as the kid from the neighbourhood next to his that stuttered, too.

Three weeks later, I read his death announcement in the local newspaper headed by "Life wasn't always very kind to you."! You can imagine that I was a bit shocked. It was clear to me that he committed suicide, though I don't know for sure, of course. My educated guess is that his severe stuttering had a major impact on his decision. He probably felt helpless, no means of communicating and expressing himself, and no good job perspective, maybe he was unemployed. God knows. I am wondering whether I could have made a difference? By chance, in a whim of a moment, I changed my plan not to talk to him. I don't feel guilty, as I did not make him stutter. But still, maybe I could have given him hope... A small difference might have made a huge impact on his life, or maybe not?

Only a sampling bias?

Scientific research is full of traps, especially regarding the use of biased samples. For example, the first polls in the US started in the early 1900, I think. And they got the prediction completely wrong, because they took voters out of the phone directory. But in early 1900, only wealthy people had phones and so they completely missed the non-phone population's political views which not surprisingly happen to be the opposite. And the candidate low in the polls won with a landslide. This post is about a possible sampling bias that creates an effect that looks intriguing and surprising, but is probably not.


Have a look at this paragraph:

"In the group of stuttering preschool children in the study summarized above (Yairi&Ambrose, 1999) their expressive language abilities were measured. The group with early onset stuttering, who entered the study at age 2-3, showed syntactic abilities and length of utterances well above what was expected for... In fact, in some aspects the language abilities in this group were on a level with the norms for 2 years older children. This was true both for children who recovered and for children who persisted to stutter. Children who entered the study at a later age showed language abilities at about age expectations, except for the group of children with persistent stuttering in the oldest age group (entering the study at age 4?5), whose abilities were somewhat below the norm. These results indicate that children with early onset stuttering tend to show precocious learning of language."

So does early language development causes stuttering? This is also what I was asking myself, but it didnt make too much sense to me. I heard many people quoting this study and another one by Rommel et al. (In Montreal, I went to see a Radiohead concert with Rommel.) But now I believe that this finding might be nothing else than a sampling bias effect. On the STUTT-L mailing list, Don Luke made an interesting observation: "This would make sense. All these children began stuttering upon reaching the same point in their development of language skills."

Here is my argument:

1) Let us assume that stuttering starts at a certain stage in the development (of language and speech skills). This is a very reasonable assumption to make.

2) Children naturally fluctuate in their development; some are earlier than others, but starting early does not mean having superior abilities later.

3) So the early-starters hit the critical stage first where they are vulnerable to stuttering!

4) So early-onset stuttering kids have early development and therefore superior-than-peers language skills at that age (but not necessarily in adulthood)


So I hope you can see that this is a pure statistical effect that has nothing to do with a direct casual link to stuttering. There is only a correlation. It might also be that late-starters go through that stage too late to start stuttering for whatever reason.

DISCLAIMER: I have actually not read the articles in detail, so I might start from a wrong premise, but the stats argument must be correct as it is maths.

More intelligent?

I am virtually convinced that a well-designed experiment will NOT show any link between stuttering and intelligence.

The only arguments I could come up with that there should be a link are

1) IQ is partially due to the environment, and a person who stutters reacts different to an environment. But this could go both ways. For example, as a teenager he withdraws and reads a lot of book or works with computers. Or, for example, his stuttering hinders him from participating in class and he is turned off by learning.

2) Stuttering is sometimes part of serious development problems in kids which lead to mental retardment. This would drag the average IQ down. But they are not typical stutterers.

I think the two effects are negligible. And one can also argue that 2) should not be included anyway in the sample.

Why would there be a connection anyway? What has speech to do with intelligence? Also brain imaging studies mostly show abnormality in structure and function in speech and language related areas. IQ is mostly associated with the frontal cortex.

Discrimination against men

Let me play devil's advocate.

I constantly hear that women are discriminated against based on the argument that "Women are underrepresented in X, so they must be discriminated against, because they are equally able and any lack of interest is pure social conditioning".

So lets turn this argument around.

Why are there so little male speech and language therapists? Are men being discriminated against? For example in the UK, I just know of one male SLP.

The other question one needs to ask is whether women SLP can truly understand the needs of male stutterers.

I have the impression that many (but certainly not all) fail to understand what works with men. Many (but not all) men don't want long talking sessions, they want targeted practise with specific goals and ideally in a competitive setting. They don't mind being told off from time to time.

Interesting biography

In my last post, I speculated that the main author Sarah Smits-Bandstra is Luc de Nil's PhD student. Actually I found her "interesting" biography at the end of the article. Such short biographies are typically intended to present the author's academic background and research interests. Here it is:

Sarah Smits-Bandstra is a registered Speech-Language Pathologist and a doctoral candidate at the University of Toronto. She is married and has a beautiful baby boy named Reid. Her research interests include the neural mechanisms of disfluent speech, and stuttering treatment effectiveness in preschool and school-aged children.

She is clearly in "a chemically enduced form of madness" (citation by Rita Carter from her book about the human brain when talking about human love). I am wondering whether my mother would go to lengths to claim that a) she is married and b) has a beautiful boy named Tom? But then again she is 60, off the hard drugs and much wiser. :-)

What does it mean?

I found this very interesting article on PubMed: here.

Luc de Nil has done a lot research in the past. I am aware of his brain imaging studies, and research on dual tasks. Webster was the first to show that people with PDS are less good at dual tasks. In their article they conclude that people with PDS take longer to automatise finger sequences. The first author is probably one of Luc's students or researchers.

"The present study compared the automaticity levels of persons who stutter (PWS) and persons who do not stutter (PNS) on a practiced finger sequencing task under dual task conditions. Automaticity was defined as the amount of attention required for task performance [Parasuraman, R. (1998). The attentive brain. Cambridge, MA: The MIT Press]. Twelve PWS and 12 control subjects practiced finger tapping sequences under single and then dual task conditions. Control subjects performed the sequencing task significantly faster and less variably under single versus dual task conditions while PWS' performance was consistently slow and variable (comparable to the dual task performance of control subjects) under both conditions. Control subjects were significantly more accurate on a colour recognition distracter task than PWS under dual task conditions. These results suggested that control subjects transitioned to quick, accurate and increasingly automatic performance on the sequencing task after practice, while PWS did not. Because most stuttering treatment programs for adults include practice and automatization of new motor speech skills, findings of this finger sequencing study and future studies of speech sequence learning may have important implications for how to maximize stuttering treatment effectiveness. Educational objectives: As a result of this activity, the participant will be able to: (1) Define automaticity and explain the importance of dual task paradigms to investigate automaticity; (2) Relate the proposed relationship between motor learning and automaticity as stated by the authors; (3) Summarize the reviewed literature concerning the performance of PWS on dual tasks; and (4) Explain why the ability to transition to automaticity during motor learning may have important clinical implications for stuttering treatment effectiveness."

I still don't understand how it can fit into my picture of PDS. Weak connections between speech and language areas cannot explain these findings. It is possible that both the weak connection and the lack of automaticity are both caused by something else.

From my experience, I certainly have trouble automatising sequences fast and loose such automatisms under stress quickly. I remember that I had especially trouble learning all the katas (a set of exercises, a bit like a dance) in Karate...

Can you detect past stuttering?

Let's assume I give you speech samples of 100 stutterers, 100 "recovered stutterers", 100 people who stuttered as children, and 100 "normal" people, but I wont tell you who is who. Can you accurately put them in the right category?

I would guess that the distinction becomes clearer the more demanding the speaking situation: from reading to talking while doing other tasks.

I believe that you can distinguish the "recovered stutterers" vs "normal" people quite accurately. I often hear "recovered stutterers" who are fluent and communicate well, but still you can sense they struggle more and speak more controlled, less spontaneous and ironically too fluent without natural disfluencies!! :-)

The interesting question is whether you can distinguish between people who stuttered as children and those you didn't stutter as children. Is it possible to detect a difference? I guess that it might be possible but only by severely stressing their brains... If it is not possible, either stuttering is just a learned behaviour or the brain completely compensates for a weakness.

1000+ visitors!!

OK. I admit that I am a bit of a Web counter junkie. I regularly check the hits and from where the people are. So I am happy to see that more than 1000 visitors read my blog in January, though these are not unique visitors. I have around 40 visitors per day with a mix of daily and weekly regulars and people stranded on my shores in cyberspace thinking what the hell is he talking about. I dont expect the number to go up much, as I am really catering for a minority of a minority, for the more research-oriented from the stuttering community. I guess I could get more reader with more emotional topics and more personal stories. But I am not too turned on with such matters!! I am a scientist at heart and obsessively curious at what is going on with people having PDS. But I try to make it sexy! ;-)

On cost-benefit & devils

In economic theory, you have the concept of benefit versus cost. Everyone wants to maximise this ratio, the most benefit at the lowest cost.

So let me ask the people with PDS the following question. Contrary to what I have been saying there is a cure (but just for this paragraph and then there is no cure. OK? :-)

The cure is quite simple: you need to do a daily exercise and then you are completely fluent for the rest of the day.

If the exercise takes 5 minutes, would you do it?
If the exercise takes 15 minutes, would you do it?
If the exercise takes 30 minutes, would you do it?
If the exercise takes 1 hour, would you do it?
If the exercise takes 2 hours, would you do it?

What is your tolerance? I think mine is at 30 minutes. And 1 hour if I can skip days and only use it if I really need it.

So now there is no cure. OK? But now I am the devil, but just for this paragraph, OK? :-)

So I am Devil Tom, and I have real superpowers. Do you want to make a deal with the devil?

Would you like to exchange your stuttering for your little finger? for a leg? for being blind on one eye? for being deaf? for being less intelligent (assuming you are intelligent)? for being ugly and oversized (assuming you are not)? for the house that you own? for your wife? (be honest with yourself! but dont tell her)

But unfortunately, I am not a devil.... at least not with superpowers. ;-)

Bad theory good outcome

I dont have a lot of time today, so a quick thought of the day: A therapy based on a bad theory might well produce positive outcomes. You might well be wrong of what causes stammering, but if you work on breathing, non-avoidance, and general control of symptoms, you become more fluent!!!

So often people say I am cured because I did A and B which followed from my theory of stuttering, but this is a logical fallacy. Other theories might also get to A and B!!!

Someone is not happy

Oh oh... someone is not happy with Andrew Bell's claim for a cure: see here. I have the impression we have another candidate for the Crackpot Award, though I am not yet convinced that he doesnt know better or is just out to make money.

Top 10 Outings

If you absolutely have to reveal your darkest secret, here are TheStutteringBrain's choices.

1) I am a stutterer. What do you do?
2) I stutter, but I am not the only one.
3) I live with a stutter but not with my parents anymore!
4) I st--- you know what I mean...
5) I am not quite as fluent as you, my dear.
6) You are so beautiful you make me stutter.
7) I was part of the Monster study.
8) I was a method actor for a Hollywood movie on stuttering but they took Tom and I kept stuttering.
9) My mother gave me gene Xi-362 - bitch.
10) I am the re-incarnation of a recovering stutterer's soul from the psychodelic 60s when he still stuttered!

Let me know if you have more.

What's the name?

On the STUTT-L mailing list was a long discussion on how to call us. The choice was between "People who stutter" and "stutterer".

These expressions might be OK for superficial use, but are quite sloppy and inaccurate expressions, because

1) non-pws stutter occasionally,
2) pws are sometimes not stuttering,
3) some pws rarely stutter but avoid,
4) most children who stutter do not become pws,
5) and people having had a stroke stutter but differently!


The term "stuttering" is also quite ambiguous as it refers both to

1) the main symptom of the disorder i.e. "dysfluent speech" and
2) the disorder itself,

leading to endless confusions.

I think "stuttering" is best left to mean the main symptom of the disorder i.e. "dysfluent speech" plus possibly secondary symptoms, and the disorder should be called "persistent developmental stuttering" (PDS), which makes the distinction between two related but different disorders non-persistent stuttering (childhood stuttering) and non-developmental stuttering (due to a neurological incident like a stroke). And then the "pws" are people with PDS, or possibly having or suffering from PDS. More on this post on my blog.

Per Alm mentioned two other expressions to me: dsyphemia, and gluency:

"I think the old concepts of "dysphemia" and Van Riper's "gluency" are relevant here – see my thesis page 22. However, I have no clear opinion about what terminology to use. For example, I do not think dysphemia is a good word but I think we would need a word for that concept".

And he betrays me by saying that

"For example, I'm not using the concept PDS very often because I think there is no sharp division between PDS and "acquired stuttering", with onset after for example head injury. I think the number of neurological lesions in "developmental" stuttering has been underestimated. "

Two types of habits

There are two types of habits than influence our stuttering: automatic and cognitive habits.

An automatic habit is a process that runs independently of an executive order by the person. You might be choking when swallowing a pill, getting nervous when the phone rings, looking down when you have a block, word substitution when you cannot say a word. This process is more or less automatised, and cannot be controlled at all or only with outmost focus, attentation and energy. You can force yourself to look into someone's eyes while blocking, but it is very hard if you have always looked down. Such habits are really programmed in your brain, most likely in the amygdala that says in "Situation X -> do Y without asking for permission by the cortex". Without such functionality, our life would be a nightmare.

A cognitive habit is an habitual way of thinking about the same situation without really thinking. Examples: I need to do a phone call I will ask my partner to do it, They want me to speak I will say no, When I call someone I will stutter, I will never be more fluent, Without my stuttering I would have achieved more. All these habitual thoughts are done without any pressure from a situation, i.e. there are no 50 people looking at you or the person on the phone is waiting or you are feeling a block coming. No, you are under no pressure, but you have pre-prepared lines of thoughts for certain situations.

Cognitive habits are easier to tackle by re-thinking one's constructs. Automatic habits are much more difficult to change.

In defense of Johnson

Instead of commenting on the study, let me take on the role of Professor Johnson's lawyer defending my client.

"Professor Johnson is shocked by the vicious smear campaign againt him from
former colleagues who now suddenly question his professionality. Throughout his
professional life as a hard working and well-respected university professor,
Professor Johnson has sought to advance our scientific understanding of
stuttering, and provide people, and especially children, who stutter with the
best care possible. His insightful research project has been a turning point in
improving treatment for stuttering and widely applied even 50 years later.
Moreover, it is important to note that this project has only come after years of
fruitless search for a neurophysiological cause for stuttering. Unlike many of
his colleagues, Professor Johnson had the courage to realise that the hopes for
a neurophysiological cause were unfortunately unfounded, and had the courage to
develop a new theory, namely that stuttering is of psychological origin, which
is supported by facts. Therefore, together with other experts including
statisticians they developed a carefully designed and monitored experiment to
test the theory. When Yairi and Ambrose attacked Professor Johnson's project in
The Journal of Fluency disorders, they not only had to base their arguments on
second-hand information, but were inconsistent in their criticism. They claim
great danger for the children, but at the same time claim that no children were
harmed and none became adult stutterers! This in fact shows how carefully
Professor Johnson's team has been! In fact, probably due to a lack of proper
research of the topic, they have missed a crucial element, namely that Professor
Johnson has made sure that the children immediately received special care after
the end of the trial. Moreover, he has even stayed in contact with some of them,
being a mentor and friend for years to come. As a parent of two kids himself,
Professor Johnson has always sought the best possible for his patients and
points out that his scientific work has been able to bring improvements in the
life of people who stutter. He finds it unfortunate that certain quarters of
academia and therapists are still clinching to a neuro-physiological cause,
which is unfounded by facts!" (Disclaimer: This text is a work of fiction, and does not represent anyone's view not even the author's!!)

Go ahead what would you say to Johnson's lawyer's statement?

The Monster study

Have you read about the Monster study? Check out the wikipedia entry:

In 1939, a controversial study on the possibility of "creating a stutterer" was conducted by University of Iowa speech pathologist Wendell Johnson and his graduate student Mary Tudor. The study tried to create stutterers over the course of 4 months, using 22 unwitting orphans from the Soldiers and Sailors Orphans’ Home in Davenport, Iowa. Ethically acceptable at the time, it was designed to induce stuttering in normally fluent children and to test out Johnson's "diagnosogenic theory"—a theory suggesting that negative reactions to normal speech disfluencies cause stuttering in children. The study divided the orphans into 3 groups: 6 normally fluent orphans would be given negative evaluations and criticisms regarding their speech, another group of 5 orphans who allegedly already stuttered would also receive that treatment, and the remaining 11 would be treated neutrally. The study concluded that the children given negative evaluative labeling went on to develop persistent, permanent stutters. The study was influential at the time, with many speech pathologists and child-health and educational professionals accepting Johnson's theory. In 1988, Silverman first reported the results of this study in the Journal of Fluency Disorders and labeled it "The Monster Study." While the information was well known to professionals in the area of stuttering, it was not until 2001 when the information was distributed to the public in a newspaper article. In June 2001, the San Jose Mercury News revealed this study to the public for the first time, leading to widespread controversy and debate about scientific ethics. Soon after, University of Illinois professors Nicoline Ambrose and Ehud Yairi wrote a paper discrediting the 1939 study, revealing flaws in data collection and method, as well as pointing out that none of the orphans actually did develop a permanent stutter. While criticism of a developing child's speech can certainly make a present stutter worse, it does not create a stutter.

My comments in my next post!

Mail from a stuttering poet

Today, I got an email from a stuttering poet! He was inspired by my discussion with Andreas Starke (see here) on a German discussion forum

His poem "complains" that during our discussion we treated people as a number and not as people! So I wrote him a poem back! Here it is. Dont be too critical with me. It is my first poem! Sorry it is in German...

Der Klippel auch wenn er's nicht gerne mag
lebt auch als Sammlung von Atomen Tag fuer Tag

Er verspuert sich wohl als stotternde Einheit,
Ist berueht von deren Geistes und Seelesfeinheit.

Doch, bitte schoen, soll er nicht vergessen,
Wer der Krankheiten weiss sich zu messen.

Es ist die Wissenschaft, die stets rational
Sich erweist des Unerklaerten Todespfahl.

Drum soll er uns streiten lassen,
Und vor unserer Aufopferungsgabe erblassen!

Le poete Tom

Why did the window break?

I read an interesting paragraph on causes, which really makes me question whether anyone who talks about causes of PDS actually knows what s/he means by "cause".

The author asks "Why did the window break?", and offered the following answers

A) "Because the brick hit the window.",
B) "Because Tom threw the brick.",
C) "Because the window glass was brittle."

He also gave the following definition: The English ‘cause’ suggests efficient causation, some factor present in a situation that actually brings about a change

This makes me think that causes can be classified

1) Into EVENTS or STATES. Event: Brick hit the window or Tom threw the brick. States: Glass was brittle.

2) Into HOW CLOSE TO "breaking the window". For example, The brick hitting the glass is a more direct cause than Tom throwing the brick.

3) Into WHETHER THEY ARE SUFFICIENT to "breaking the window". Some causes are a necessary but not sufficient conditions for the change "window breaks". For example, the glass needs to be brittle for it to break, but you need some extra i.e. the brick hitting the glass.

So "Why do people stutter?"

Getting rid of a habit

We all know that therapy also involves unlearning bad and unnecessary habits. Not being able to say a word is one thing, but avoiding eye contact, speaking faster, body grimaces and being tense in order to somehow avoid stuttering is not only unnecessary and doesnt look cool, but is contra-productive and actually makes a block worse. I think all people with PDS can agree that these habits are unnecessary, but then again once in a block we just cant prevent the habits from being executed by this vicious part of our brain that overrides our executive orders. I want to tell you the following story illustrating how difficult it is to get rid of a habit.

As a kid I was good at sports. But, I was terrible when it came to swimming. I couldnt swim well, not because I was unfit, but because I was not able to apply the breathing techniques well to do crawl. Why? I somehow developed this habit of choking when I tried to breathe into the water. So after a few strokes, I couldnt continue and gasped for air. Four years ago, I started swimming regularly. It took me nearly four years to get rid of this choking habit. Now I can swim crawl without problems. Parodoxically, even when I try to choke, I cant anymore... The unlearning of this habit came very slow.. Stage One, I tried to change and the choking was worse. I hated swimming crawl. Stage Two, I was able to swim longer without choking, but still experiencing a feeling of being uncomfortable and of having to choke any second. Stage Three, once a while I started choking again, and I was pissed off and switch to breast stroke. Stage Four, I was able to swim without choking, but still felt a bit nervous. Stage Five, I just swam without thinking about it. Stage Six, I realised that I conquered it and saying to myself "I got you. Come on. I challenge you. Make me choke!" I can now confirm that I am a recovered choker, but I am not sure whether I am cured! :-)

I hate to think that unlearning stuttering habits is probably even harder...

Are you a crackpot?

I am not sure whether you know what a crackpot is. According to wikipedia, Crackpots are: "Pejoratively, the term Crackpot is used against a person, who writes or speaks in an authoritative fashion about a particular subject, often in science, but is alleged to have false or even ludicrous beliefs." They are especially common in my home field of theoretical physics. Either they claim to have disproven Einstein, or have found the laws of physics that unify all fundamental theories from quantum mechanics to general relativity. A negative response from the physics community often leads to claims of conspiracies. Examples are here, here, and here. When I was a visiting researcher at DAMTP (the institute where Prof Stephen Hawking works) at the University of Cambridge, the news went around that a Japanese person called up Hawking in the middle of the night: "asking to talk to the prof to tell him that he had solved all mysteries in physics". I also had my share of crackpots. It is virtually impossible to convince them why their theory is not correct. Here is a test for physics.

So how about in the field of PDS? Here is Tom's ...

Are you a crackpot? test

1) Do you have a cure for stuttering?

2) Have you cured yourself from stuttering?

3) Did you have an inspirational moment, where suddenly you instinctively you knew what stuttering is really about?

4) Do you often refer to big names to agree or disagree with them like "I agree with Freud that..." or "I disagree with van Ripper that..."

5) Do you dismiss brain imaging and genetics studies as irrelevant without having read the research articles?

6) Do you think that people ignore your ideas to protect their own interests? Or that there is a secret conspiracy against you and your ideas?

7) Do you firmly believe that PDS is purely psychological?

8) Do you write a blog making comments about PDS research even though you only have a PhD in theoretical physics? (quote from a university professor)

9) Do you talk, talk, talk, talk, talk, talk, talk, talk, talk about your experience instead of asking others about theirs?

10) Do you over-use words like holistic, in-touch-with-oneself, and so on?


If you have answered more than three questions with YES: Congratulations!, you are a crackpot! :-) Please note that a university degree or a professorship does not neutralise the results, as experience shows in physics.


Here are the solutions:

1) There is no cure that works for everyone.

2) You might well have become fluent through hard work or / and an X event, but you are not cured in the sense that you have the same speech system as normal people.

3) You might well have had such a moment, and as a consequence became more fluent, but that does not mean that you understand PDS. You can very well become fluent by using a wrong theory of PDS. Like someone who thinks the treatment is a cure will be more successful that Tom who knows about relapse and so on.

4) Science is about strength of arguments and not about who made an argument. Personally, I couldnt care less about who said what. For example, in my field of physics, I have never heard any of the world leading people say "Einstein said that...". All the so-called authorities in PDS are just human beings who also make mistakes. And then again, why does someone become an authority??

5) Dismissing this kind of research without trying to understand it is just insane.

6) They might well protect their interest, but that doesnt make your theory right! Because if your theory is wrong, they would have behaved in the same way!

7) There is now so much research on brain and genes that this position has become untenable.

8) :-)

9) If you start talking to other people, you will realise that your stuttering is very different to others, and that generalising your situation or building a theory only on your experience is not possible.

10) These terms are very vague and not useful for a scientific discussion.

More fluent at ovulation!

Here is another interesting observation of the strange aspects of PDS. Per Alm pointed me to a study of the menstrual cycle, showing more stuttering during the premenstrual phase! This clearly points to neurotransmitter (brain chemicals) levels in the brain affecting fluency. So PDS cannot really just be psychological, because the menstrual cycle is related to changing hormone levels?

Silverman, E. M. (1975). Speech fluency fluctuations during the menstrual cycle. Journal of Speech and Hearing Research, 18, 202-206.

Abstract: This study sought to determine whether changes in disfluency characteristics accompany biological and emotional changes during the menstrual cycle. Four extemporaneous speech samples were collected from each of 12 women, one at ovulation (when the average woman experiences her greatest feelings of self-esteem and self-confidence) and one at premenstruation (when she experiences a significant increase in anxiety level) for two consecutive cycles. The mean total frequency of the women's speech disfluencies produced at premenstruation was significantly greater than the mean total of their speech disfluencies produced at ovulation. The disfluency type that accounted for much of the difference in total frequency of disfluency between the two cycle points was revision-incomplete phrase. The tendency for these nonstutterers to produce more speech disfluencies at premenstruation than at ovulation is similar to a tendency we have observed in stutterers

Silverman, E. M., Zimmer, C. H., & Silverman, F. H. (1974). Variability of stutterers' speech disfluency: the menstrual cycle. Perceptual and Motor Skills, 38, 1037-1038.

Abstract: Studied whether women who stutter produce more speech disfluencies at premenstruation (when anxiety level has been reported highest) than at ovulation (when anxiety level has been reported lowest). 4 speech samples were collected from each of 4 Ss, one at ovulation and one at premenstruation for 2 consecutive cycles. Results show that Ss produced more disfluencies premenstrually.

Time line of discoveries

In my last post, I talked about the maximum understanding and treatment that is possible in the future.

Here is Tom's oracle for major research events in 2006 and what they will find:

1. Brain imaging studies of teenagers, children who stutter, and adults who have stuttered as children: They will probably show that structural abnormalities already exist from very early onwards, and that children and adults who recover also have structural abnormalities.

2. More detailed genetics studies: Past studies have localised the responsible chromosomes for specific cases. They will localise the genes on these chromosomes. The function of the gene(s) will probably be building a protein that is (partially) needed to direct the development of language and speech areas in the brain.

3. The pagoclone study: The results will be very mixed. Some experiencing great improvement, but other none at all. Side effects will exist but relatively small. Leaving everyone do wonder why the hell it works for some and not for others? The company will probably go on with the next phase of trials, but instead of a cure they will focus their message on "Pagoclone works for some very well and for others not at all. You need to try it out with your doctor to see whether it works for you."


Within the next five years, 2010:

1. Medication (possibly Pagoclone or others) will become available. It will prove not be a perfect cure, but alliviate severity for most and considerably for some. There will be more clues as to why medication works for some more than for others. Possibly subtypes are identified by other means, or effect of medication will be used to define subtypes.

2. Brain and genetics research is now 15 years old, and the field will have come to a consensus on the broad features of PDS within the brain and the genes.

3. Meta-analysis is finally becoming more important in fitting everything together, because by now experimental evidence is detailed and plenty enough to be able to construct good theories.

4. Most early baby-boomer professors / therapists with old (anti-brain and so on) ideas will finally be in retirement leaving the way open for new people. (I do not mean all professors, just some! :-)

5. Other brain disorders will have been sorted out giving clear directions on within which framework to think about PDS.

Understanding and treatment in 9999

Pablo from Spain asked me some time ago: "Do you believe that in our life time (I am 36) there will be a truly scientific understanding of stuttering and a truly scientific therapy for curing it?"

Let me first say what I believe is the maximum understanding and treatment we can achieve: (I will talk about timeline in my next post)

1) PDS is very likely not a local problem but a more distributed problem. I give an example: it is not like computer hardware breaking down due to a faulty cable or a software with a bug in the code, but it is more like a very inefficient transport system or a high crime rate in a city. You will never be able to answer the question: Where exactly is the problem? You see the effects, but many factors play a role like the underground trains are very old, only one underground line, and the unions block any change. Currently, we don't even know what the various factors are. It's like, the city is still very foggy, and we slowly need to get rid of the fog (also due to genetics and brain imaging tools) and explore the different factors. The maximum understanding will come when there is no fog anymore, and all factors and how they interact are known.

2) There will not be a cure in the sense as having the same speech system as normal speakers, but more like the children who have recovered. Much greater fluency will be achieved faster with fewer relapse. Thus, it will not be like the computer doesn't work due to a cable failure so lets replace the cable or the computer bug is here lets replace this line of code. It is more like lets improve the inefficient transport system. God knows where you should start. So build a new underground line or lets get new trains. BUT the problem is that you cannot shut down a city (or a human being) for a few months and re-build everything. You can only do slow step-wise improvements. In therapies you always need to work on a change in behaviour, but with no fog around the city anymore, we will know much better where to attack the problem (which might be slightly different for different people). Medication is probably the most straightforward way to help people, as you just take a pill and nothing else. You don't need to follow some therapy which is much harder. Taking a pill will change neurotransmitter level in the brain and is like ensuring that there is never bad weather in the city or the people using the transport system are not stressed. And the transport system improves tremendously (without solving underlying issues), but is not really a cure as such.

Actually, to be completely honest with you, I think that in 9999 there will be no human beings anymore as we know now. So there will also be no stuttering anymore!! We will have morphed with computers into one big system. We will be sub-entities like cells in our body. And communication between sub-entities (direct descendants of us) will not involve speech anymore. This process has just started with the Internet. For example, take my blog, I am currently putting ideas into your mind, and you can influence my mind by posting comments. These comments are just like my own thoughts: I might take them on or ignore them. Wikipedia and google have also dramatically increased our common shared memory and so on. This process will continue... :-)

Is PDS research as exciting??

Here is another interesting talk on preliminary brain imaging results by Kell, Neumann, and Giraud: I know Katrin Neumann and I have spoken to Anne-Lise Giraud once. I googled Christian Kell, and he is most web-famous for scanning the cortex representation on the penis! See here. Apparently, the region is very small! (contrary to the commonly presented picture! See above) Dispelling the terribly dangerous myth created by sexist females that men are controlled by their... I am wondering whether Kell finds his research of PDS as exciting?! :-)

The researchers from Frankfurt claim that prosodic production tasks during fMRI reveal functional deficits in stutterers. Prosody can be defined as the patterns of stress, intonation and timing in a language. They say that both groups with or without PDS show similar performances, but have different brain activation. I am not sure what to think. From my personal experience, I seem to be far more fluent when I actively control the prosody of my speech. It feels a bit like singing, or chorus reading. So even if abnormal, the prosody neural network seems to help me to be more fluent. But of course, this might only be the case when I actively control my prosody and on automatic mode it becomes unstable? How does this fit with the dual premotor systems hypothesis Per Alm has been advocating: see here? Not sure how their results would fit in. I don't think they have published the findings yet. I guess they are in the review process.

Here is the abstract:

Persistent developmental stuttering can be interpreted as the result of impaired linguistic motor executive function. Previous studies revealed pathologies in somatomotor as well as language-related cortices of stutterers. Frontal opercular regions (Broca and its right-hemispheric homologue) appear differentially activated in stutterers when compared with healthy controls. Stutterers seem to compensate their defect spontaneously via an activation of the right frontal operculum, while after fluency-shaping therapy a more left-lateralized frontal activation can be observed. Based on these findings, we sought to preferentially activate either the left or the right frontal lobe. Prosody perception usually involves lateralized cortical networks depending on whether it emphasises linguistic or emotional features. We therefore hypothesized that a similar functional lateralization should be observed in frontal regions during speech production emphasizing different prosodic features. While production of linguistic prosody should predominantly activate left-hemispheric regions, emotional prosody should reveal a more right-hemispheric network. The production of linguistic prosody should therefore reveal in a very selective manner relative left-hemispheric deactivations in stutterers, while production of emotional prosody should tell us more about the functional meaning of right frontal overactivations in stutterers relative to controls. After confirming functional lateralization of spoken prosody in normal subjects we compared activations in stutterers and controls. Despite similar behavioural performances, we found a very circumscribed left frontal deactivation in stutterers in the linguistic prosodic task in BrocaÂ’s area. The emotional prosodic task activated larger fronto-temporal networks in stutterers, but no significant differences were found in the group analysis. Our results delineate a focal functional lesion in the stutterersÂ’ left language executive network, which may require compensation by BrocaÂ’s right homologue.

Blog of the week

Check out the Genetics & Health blog by Hsien Hsien Lei. The Stuttering Brain is the blog of the week. :-)

Tom vs RCT: 2nd round.

Some time ago, I discussed the Lidcombe random control trial (RCT) and why I believe they need to revise their statistical measures: see here, and here.

Mark Jones et al. have responded to the rapid responses, but they have not directly responded to the arguments put forward in my rapid response. For example, they say that

"... spontaneous recovery has been a recurring theme in the rapid responses to our article... The rate of natural recovery from stuttering in young children in the general population has been estimated at 74%(1), but in clinical populations with this condition this estimate is expected to be much lower...Evidence from a previous study(2) suggests that approximately 40% of children identified as stuttering had the condition for less than 6 months."

However, they do not directly relate this or other statements to my arguments to disprove my case, so it is difficult for me to respond in a constructive way. My guess is that they imply that any effect due to the spontaneous recovery rate on the statistics is very small because the rate in the clinical setting is only about 40% and not about 75%. But this argument is not correct. The great irony is that the closer the recovery rate is to 50%, the greater the impact on the statistics!! :-) So by claiming a 40% rate instead of a 74%, they have actually strengthened my argument that they need to revise the statistical significance and effect size of their study to take into account the natural recovery rate!

I have sent a response, where I explain in more details. The response should be on-line in one or two days. Check here.

New Year Resolutions

I forgot. I wish you all a Happy New Year.

Here are my New Year Resolutions:

1. Keep on writing posts at the same pace. Might be tough if I get more busy job-wise.

2. Try to get a few promiment researcher write a few posts.

3. Re-design the blog layout and functionality a bit. I might include a stuttering brain in the header. If you have any suggestions, feel free, especially if you are the creator the French website Paroles de bègues! :-) I am also thinking of generating a bit of money to cover my costs and time spent. I am not sure about a google AdSense button. But I might add a Donate button in case a millionaire wants to donate some money! :-)

4. I am also thinking about launching a website to include a discussion forum on research, archive, lists of researchers, and more. I have already a precise idea and a project plan. But just need the time and focus to do it. Maybe it would be good to get more people involved in such a project. But teams (and committees) are typically nightmares and compromises virtually always worse outcomes that either of the two competing proposals!

5. To be a bit more serious on reading the PDS literature.

All my posts of 2'005

I have created a file that contains all my posts of 2005. The file is a .mht archive format, which any browser reads. You can read the document by clicking here.

The file is accessible from a link I added to Archived Posts: see on your left, scroll down a bit.

Over time fluency

I am wondering whether some research has recorded the fluency over a long period of time on a daily basis: How much is the fluctuation? To which factors is it related? Are there people who fluctuate much more dramatically? (For example, I remember giving a talk in near complete fluency and many in severe stuttering) Why? Do men differ from women? For example menstrual cycle?

I did an interesting test. I took the data from all the patients of the Kassel Stuttering Therapy database, and plotted their fluency data with respect to the month they were recorded to see whether there is a seasonal difference. For example, may be we stutter more during the winter then the summer? But I did not find any strong signal, but this might due to methological problems. The data is not well normalised, i.e. some months might have more severe stutterers.

My paradigm shift

I have subscribed to the STUTT-L (see FAQ on STUTT-L) as you don't leave a lot of posts, and I get bored!! :-) On the first day, my mailbox was FLOODED by pretty low-information content emails, but there are also an interesting discussion.

BUT Per Alm's following comment has triggered a paradigm shift in my thinking:

What is important to point out is that observations of other possible impairments, for example of language ability, very well may be an "epiphenomenon", that is, a phenomena that occurs in parallel with stuttering but that is not causally related to stuttering. All too often reports of differences between stuttering and non-stuttering persons are interpreted as causal, when they are more likely to be just epiphenomena.

In the back of my mind, I always thought of the lower performance of people with PDS in dual tasks like finger tapping (research by Webster, de Nil and Bosshardt), and language skills (research by Christine Weber-Fox) as collateral damage to PDS. I never gave it too much importance. But now suddenly I find this research and the related insights very exciting, very important and crucial for the bigger picture of PDS! Why?

My current thinking (and of the few people with the same wavelength) often is based on two views:
1) We concentrate on stuttering either as the symptom of overt stuttering or concentrate on the brain mechanism that leads to stuttering.
2) We view stuttering as the disorder, and PDS causes or also includes much more subtle deficiencies like dual tasks, language deficits, etc.

But now I think that is a very biased way of looking at the issues. And the two views should be:
1) Overt stuttering is a (but not necessarily the only) consequence of PDS and PDS is a (but not necessarily the only) consequence of X.
2) X causes many different functional deficiencies like PDS, language deficits, dual task deficits, and possibly more. PDS is only the most visible due to its importance in human activities, and a compensating mechanism only works well in 80% of the cases but only partially compensates in the remaining 20%. Then the 20% face enormous pyschological and social pressure, because they do not function normally, "normally as defined by the environment they live in" and their reaction to their stuttering is very strong leading to even more severe stuttering, bad habits, and so on. Were subtle dual tasks as crucial for human activities like speech, we would be dys-dual-tasking.

X is a structural deficiency/abnormality happening during the development of a brain region(s) caused either internally by genes or externally by some neurological incidents (or even due to some rare extreme traumatic experience).

X exists in all developmental brain disorders. X can happen in all kinds of brain regions due to all kinds of genes leading to different disorders. X may cause or increase likelihood of development of PDS, dyslexia, and dyscalculia (spelling?), for example. Everyone has some X somewhere, but often the structural deficiencies lead to non-detected subtle functional deficiencies, because they are not important for our functioning (in our society). For example, 10'000 years ago no-one would have cared about dyslexia, and there would have been no opportunity to see it in a society without writing and reading! So X is not really a disorder as such but just nature experimenting with different gene setups. And the society and the environment will select out genes that cause the Xs which lead to significant handicap impairing chances of re-productivity.

OK. I better stop here. I will read this post again tomorrow to see whether this is all nonsense or a beautiful new paradigm of looking at PDS. :-)

3-group race

This is my last post on brain studies of kids.

As far as I know, there are three groups that are actively recruiting and scanning kids. The group around Katrin Neumann at Frankfurt, Kate Watkins at Oxford, and Soo-Eun Chang at NIH. All three groups are linked to "scanning factories" with considerable experience and expertise. So the research should be of a high scientific standard.

Sofar, just Soo-Eun Change et al. have communicated preliminary findings, as I have discussed here and here.

Once all three have published papers, which as always might take years with the secretive, out-dated, time wasting and often pretty useless current peer review process (that could not even deter the significant fraud of Prof Hwang on stem cells), the fog will clear further, and we will have a much better understanding on how PDS works.

Related fields do our research

Science has nominated the Breakthroughs of 2005, and better understanding of genetics of brain disorders has been a runner-up: see here. This is very exciting news, very possibly of relevance to PDS. The findings provide us with a constructive framework within which to think and then adapt to fit PDS. Science says: Much of the new work suggests that genetic miscues, rather than causing neuropsychiatric disorders outright, alter brain biology in the womb in a way that predisposes us to problems later in life. A better understanding of how this happens may help reduce the risks. It is very likely that PDS fits into this category.

There are two reasons for better progress in neighbouring areas. Much more money is going into these areas (dyslexia, schizophrenia or Tourette syndrome), and research is generally more scientific than in PDS and not as laden with foggy swampland of psycho-stuff for several reasons. I also think that it is a scandal that so much money has gone into other brain disorders and so little into PDS. We need to shout louder when it comes to getting a share of the research money!!! Remember when you shout, you don't stutter!!! So start shouting! :-)

Here is the description of Science:

Miswiring the Brain
Although dozens of genes have been linked to brain disorders in recent years, connecting the dots between genetics and abnormal behavior has been anything but child's play. This year, however, researchers gained clues about the mechanisms of diverse disorders including schizophrenia, Tourette syndrome, and dyslexia. A common theme seems to be emerging: Many of the genes involved appear to play a role in brain development.

In November, two reports put meat on the bones of previous claims that variants of a gene called DISC1 increase the risk of schizophrenia. One research team found that inhibiting DISC1 activity in mice alters brain development, causing subtle abnormalities in the animals' cerebral cortices similar to those seen in postmortem brains from schizophrenia patients. Another team linked DISC1 to molecular signaling pathways important in brain development and in regulating neurotransmitter levels, which are often out of whack in psychiatric patients.

In October, researchers described a rare genetic defect that appears to cause Tourette syndrome. The mutation likely causes only a tiny fraction of Tourette cases, but its discovery may be an important lead. One gene that's disrupted, SLITRK1, influences branch formation by neurons and is active during development in brain regions thought to be altered in Tourette syndrome and other conditions, including obsessive compulsive disorder. New research also links developmental genes to dyslexia, identifying three genes--KIAA0319, DCDC2, and ROBO1--that may cause faulty wiring in neural circuits involved in reading.

Much of the new work suggests that genetic miscues, rather than causing neuropsychiatric disorders outright, alter brain biology in the womb in a way that predisposes us to problems later in life. A better understanding of how this happens may help reduce the risks. (Science website)

Hurdles for brain studies in kids?

Looking at kids is probably a bit more difficult than I originally thought it would be. They are more of a moving target in terms of comparing brains between individuals. Whereas all adults have fully developed brains (and only small changes with advancing age), the younger the kids the more difference between them due to a natural fluctuation in the speed of development, even for the same age. So, comparing a 6-year old with a 10-year old is much bigger issue than comparing a 24-year old with a 28-year old or 35-year old. So really you need kids of the same age to reduce this source of error. But even then, I guess the difference between their brains might be bigger than between 24 and 28 year olds, for example.

Another brain study on kids

Here is the only other article I know about brain studies on children. The title is Cerebral Lateralization of Speech Processing in Adult and Child Stutterers: Near Infrared Spectroscopy and MEG Study, and the authors are Koichi MORI, Yutaka SATO, Emi OZAWA and Satoshi IMAIZUMI from Japan. I met Mori at the Montreal IFA conference in Summer 2002, and he gave me a copy of his work. Near infrared spectroscopy is brain imaging technology that "shines" light into the brain and analyses the light reflections.

Here is the abstract:

Cerebral lateralization of speech processing in stutterers were assessed with noninvasive brain imaging techniques, magnetoencephalography and multichannel near infrared spectroscopy (NIRS), with which neuromagnetic and hemodynamic responses, respectively, were recorded to analysis-synthesized prosodic and phonemic minimal contrast word trains. Adult stutterers did not show normal leftward dominance for the phonemic contrast with either method. Children underwent only NIRS sessions, with results similar to those of adults, which indicates that the cerebral dominance in processing heard speech is in disarray even in school-age stutterers. NIRS method may be useful in screening young stutterers and in elucidating neural correlates of stuttering.

Strangely enough or as expected, their research has neither been replicated nor commented on by the "Western establishment". To me, their findings are at least interesting enough to be criticized! :-(

More info on the kids study

Here is more information on the preliminary study, and its caveats: see also here.

Background

... These previous [brain] studies, however, have been limited to examining only adults who stutter, and no studies have thus far examined neural correlates of spontaneous recovery from stuttering. Hence it remains a clinically and theoretically imperative goal to determine the neural correlates of childhood stuttering persistence and recovery, closer to disorder onset.
Here we present preliminary results from a voxel-based morphometry study
(VBM) looking at children with persistent stuttering (CWPS), children who have spontaneously recovered from stuttering (CWRS), and children who have never stuttered (CWNS). Results indicate that, compared to CWNS, children who persist or have recovered from stuttering have significantly less gray matter density in the left hemisphere inferior frontal regions coinciding with the Broca¹s area, as well as the anterior cingulate. Interestingly, CWRS showed an intermediate level of gray matter density compared to CWNS and CWPS in these areas. Results are discussed in context of possible developmental pattern differences that lead to, or are a result of, eventual persistence or recovery from stuttering.

Discussion

The present results point to anomalous gray matter density (GMD) in several regions of the brain as possible neural correlates of developmental stuttering. Regardless of eventual persistence or recovery, children who have once stuttered appear to exhibit significantly reduced GMD compared to their normally fluent peers in areas such as the left IFG, an area known to be critical in speech motor planning. Although CWRS generally showed a similar pattern of GMD findings to CWPS, they also exhibited important differences from the latter, which may reflect brain plasticity associated with natural recovery from stuttering. For instance, CWRS tended to exhibit an intermediate level of GMD in the left IFG and ACC, namely, levels of density approximating that of controls. On the other hand, CWRS tended to have decreased GMD in parietal regions such as the SMA (BA 6) and the SMG (BA 40) compared to the other two groups, possibly reflecting the effects of increased pruning in these regions correlating with a compensating mechanism they may have adopted to aid in recovery.

This study has several limitations. First, due to the small sample size in the three groups (n=7 in each group), the results are preliminary and need to be replicated with a larger sample. Second, although VBM provides an even-handed approach to looking at regional differences among groups on a whole brain basis, the process of averaging and smoothing involved in the analysis pipeline may obscure individual differences in structure, and group differences in smaller areas of interest may be more difficult to identify. Third, structural anomalies may merely represent risk factors for anomolous function. As such, future studies may consider pairing structural techniques such as VBM and DTI with functional techniques (i.e., fMRI and MEG) in order to elucidate correlations between anomalous structure and functional deficits involved in development, maintenance, or recovery from stuttering.

First evidence of brain anomalies in kids??

I am going to send a letter of complain to the editors of The Stuttering Foundation newsletter for being more up-to-date on PDS research than this blog!

The Winter edition has pretty interesting articles and reports on research I wasnt aware of! For example, Ehud Yairi reports on brain research with children:

Brain imaging studies of children should also enhance understanding of this issue. Our team members, Chang, Erickson, and Ambrose (2005) successfully obtained high resolution structural MRI data from stuttering and control children ages 8-13. Initial results indicate significant group differences in white and grey matter volume in brain areas involved in integrating sensory and motor aspects of speech. Testing younger children closer to onset should advance our knowledge.

Reference given: Chang, S., Erickson, K., & Ambrose, N. (2005). Regional white and grey matter volumetric growth differences in children with persistent versus recovered stuttering: An MRI (VBM) study. Presented at the annual meeting of the Society for Neuroscience, 2005, Washington, D.C. Program No. 565.5. 2005 Abstract Viewer/Itinerary Planner. Online

This research (if replicated) weakens the argument that structural anomalies in people with PDS is a consequence of PDS and not the cause. I guess due to the ages, from eight to thirteen, it is still possible that it is a consequence, but no-one can now claim "No wonder the brain is different after decades of stuttering"!

Sure, there will be some effect from stuttering even in younger kids, but I think it is mostly there from the start. Something in the developmental phase around 3 goes wrong. Another article comes to my mind (of which the editors of The Stuttering Foundation are surely not aware :-) from Japanese researchers, who found differences in processing in small children with disfluencies. I'll try to dig the article for you. I think he is called Mori.

Very interesting article

There is a very interesting article by Lisa Scott on a session "Genetic and neurological correlates of stuttering" at the last American Speech-Language-Hearing Association (ASHA) conference. All four of them have done good work, and let's hope they see the need and find ways for multi-disciplinary collaboration!

Here is the introduction:

In November, four of the leading scientists in stuttering presented their latest research at the American Speech-Language-Hearing Association convention in San Diego. Participating in a session entitled, “Genetic and Neurological Correlates of Stuttering,” were Drs. Dennis Drayna, NIDCD, Christine Weber-Fox, Purdue University, Ann Foundas, Tulane University, and Gerald Maguire, University of California-Irvine. In a session coordinated by Dr. Christy Ludlow, NIDCD, four presenters focused their discussions on state-of-the-art research in the understanding of genetic and neurological factors that contribute to stuttering. Three of the four researchers, Drs. Drayna, Weber-Fox, and Foundas, have previously contributed articles on their research to past issues of this newsletter.

You will find the full article: here.

Two types of factors for recovery

The factors increasing the chance of a positive therapy outcome are still largely unknown. The only sure factor is the severity of your stuttering. So if you are stuttering severely before therapy, you are more likely to keep on stuttering than someone who has stuttered mildly. So the bigger your problem with PDS, the more likely you are not becoming fluent after therapy. But that's it! No other factors are known. That is what I found looking at the KST data, and also what others seem to find.

I am still not sure what they are. But I conclude that the path to becoming a more fluent speaker, must be divided into two types of factors:

1. PDS-Specific factors: Severity of your stuttering. And then some guesses: How big is the physical anomaly? How strong are the secondary systems? Are you naturally a fast speaker? Is your PDS due to genetics or neurological incident in childhood?

2. Other factors: Some guesses are. Are you a bit obsessive and pedantic (when it comes to applying your techniques)? Are you often emotionally suffering (from PDS and have a strong motivation to change)? Have you undergone a life-changing experience like a car accident (that seriously affected you and you decided to work your stuttering?) Can you control your impulses well? A change in some neurotransmitter cycle? Are you in the right life situation (to foccus on therapy)?

M---mmmmmerry Xmas! :-)

New twist to stuttering genes

I have decided to spend a bit more time to read up on genetics during the Xmas and New Year period, and write a popular-scientific article about the genetics of stuttering. I have been encouraged in my endeavors by the Pennsylvania court decision that it is still OK to talk about and teach evolution without reference to intelligent design. :-)

Most research on genetics and stuttering has revolved around twin studies or looking for genes or combinations in samples like families where most members stutter: see a previous post. This new article on stuttering and genetics puts a new spin on the issue and in the right direction. A gene alone is not enough, it seems. You need the right combination of genes, or the right conditions for the gene to have important effects: read about the Epistasis effect. The researchers suggest that maternal age at birth might be such a epistatic factor.

Maternal age at the birth of the first child as an epistatic factor in polygenic disorders.

The identification of the genes for complex, polygenic disorders has proven difficult. This is due to the small effect size of each gene and genetic heterogeneity. An additional important factor could be the presence of unidentified epistatic factors. In the broad definition of epistasis, the effect of one unit is not predictable unless the value of another unit is known and one of the units may not be a gene. We have previously identified maternal age as an epistatic factor for the effect of the LEP gene on the age of onset of menarche. We report here the effect of maternal age and the age of the mother at the birth of her first child (maternal age 1st) as epistatic factors for the interaction of the dopamine D1 gene (DRD1) with obsessive-compulsive behaviors and with stuttering. The epistatic effects of maternal age 1st were stronger than maternal age. This type of epistatic factor may be generalizable to many other gene-trait interactions.

The science journal Science has named new research on genetics of other brain disorders like dyslexia and Tourette syndrom as a 2005 Breakthrough topic. I will talk about this in my next post, and be desperately trying to make a connection PDS.

Arty French stuttering blog

If you speak French, you should have a look at this French stuttering blog: Parole de Bègue.





If you dont speak French, still have a look! The design is beautiful.... :-)

Pebbles under the tongue

Here is a "rival" blog on stuttering: Pebbles Under The Tongue. John MacIntyre describes his efforts to become (more) fluent with a fluency shaping therapy. Currently John is in the maintenance phase after the intensive therapy phase. Of course, this phase is critical, and often relapse happens. And a lot of patience, courage, honesty-to-yourself and stamina is needed to keep on course. Qualities I think John shows admirably in his last post:

Up until last week I had done my daily shaping every day. But last week I missed 2 days, and this week I missed Monday, Tuesday, and Wednesday. I wasn’t happy that I missed it, but life just kind of took over. By mid week I had totally lost my ability to use my targets, increasingly using my previous spontaneous fluency pattern.

But Wednesday evening, I was stuttering like a maniac picking up a prescription at the drug store…I was blocking badly. And as reminiscent of old times, the guy behind me, just had to see my face as I attempted to shield myself from the embarrassment! He started off behind me, but when I started to stutter, he came around my right side leaning over to watch me. When I turned my back on him, leaning left, he moved completely around to my left side. I turned away again, and he again moved to my right. At this point, I realized he was determined to watch, so I stopped trying to get away from him and let him watch me make a fool out of myself!

Guess what … I came home and did my shaping! I did it yesterday and today. I don’t think I’ll miss it again for a while. ;-)

I don’t know what the heck that was, but before my therapy, I definitely would have stuttered and interpreted the hang up as some kind of rejection. Then I would have felt like crap for the rest of the day. At least now I know what ever the heck the problem was … it wasn’t my problem and I quickly moved on with my work.

In this post, he has made public his before and after video. The changes are amazing, and very similar to the ones I observed at the KST. There are also videos of myself at the KST. I'll see if I can get hold of them.

Here is John's talk given at Toastmasters.

Pagoclone results in Mid 2006

The results of the pagoclone study will be out Mid next year: "In July, the Company announced the initiation of a Phase II clinical trial with pagoclone, a product under development to treat stuttering. The Company is currently on track to have results from this trial by mid-year 2006."

My past posts on pagoclone are here, here, and here.

Off to Switzerland

Upps I posted this in my other blog.... :-)

I am off to Switzerland for a week, but might post if I have Internet access. I am going to meet up with someone from the Zurich self help group. He is regularly reading my blog, and I got to know him via email.

Strangely enough, when I try to speak German with a Swiss accent, I hardly stutter ... Maybe I (or we all) should consider moving to Switzerland as a good treatment approach... But then I am not quite sure why there are still Swiss people who stutter? :-)

Picture of Tom

Some people commented that the blog is a bit boring... So I added my picture. If you cannot stand looking at me, please will you let me know and I take it off. Actually, maybe I get annoyed first about looking at my picture too often.. :-)

I plan to do a few more changes... If you have any suggestions, please let me know.

Biggest obstacles to better understanding

Here are Tom's Top obstacles to a better understanding of PDS.

Five removable obstacles:

1. missing paradigm to study brain disorders with many different interacting layers.
2. lack of rigorous scientific discussion in favour of a every-one-is-welcome and everyone's-thoughts-are-interesting-even-if-completely-wrong attitude.
3. no big money going into PDS research.
4. research field mostly populated by not-very-good or good-but-not-outstanding scientists, and by professors with money, power and good expertise but limited scientific insight. And outside researchers with insight have limited expertise in the complexity of PDS.
5. no good structure to do meta-analyis and unity all research.
6. researchers rarely replicate studies, but do different experiments.

Five obstacles you have to live with:

1. No-one dies from stuttering.
2. Brain is a complex system with many different interacting layers.
3. You can make little money from PDS.
4. Most people are victim to logical fallacies.
5. PDS is more like a high crime rate in a city than a broken down computer.

Nothing ado about hearing?

In a previous post, I described this article.

My view is very much in line with what Peter wrote: here. Actually, I am wondering who Peter is? :-) I googled "Peter stuttering". And I find a Prof Peter Ramig and a Peter Louw. I would guess it is Peter Ramig, but I have never met him.

Some more comments:

1. Their review is not very good. As you do not have the actual paper, here is one quote "individuals with PDS have... a cortical disconnection between the frontal operculum and ventral premotor cortex [reference: Sommer et al.]". Several issues here: 1) they present it as a fact, even though they only quote one source Sommer et al. 2) Sommer et al. never said such thing 3) They found a lower coherence in a fiber tract. This is either an experimental artefact or a structural weakness. But not a disconnection as such, more like a noisy phone line or a 1-lane motorway. 4) There is no direct connection between frontal operculum and ventral premotor cortex. To summarise, such reviewing practise is really annoying and encourages myth propagation. (Thx for input by Per Alm)

2. They find correlations by looking at many different variables and not by looking at the variables a-priori considered interesting. Looking at too many variables, there is a considerable chance that one variable is correlated to stuttering (for example) by chance. They used self-rated dysfluency as measure of stuttering.


As Peter says, the different reaction to changed sounds could just be a natural learned behaviour to their stuttering. But even if this is the case, does this observation not tell us that therapy needs to consider hearing issues? Or is it irrelevant?

Battle with German titan

I am currently having a discussion with Andreas Starke, the titan of German stuttering therapy on a German discussion forum.

If you speak German, have a look here.

4000 visitors!

According to my webcounter, 4000 visitors have sofar visited my blog since May. And I have 22 different visitors per day, which is pretty OK considering the speciality of the topic, and my many technical / scientifically oriented posts.

Visitors come from Europe (55%), America (37%), and the rest.

The most visitors are from the US (33%) and Germany (21%). The Luxembourg (14%) is probably mostly myself! :-) The UK representation is pretty poor, but this is actually just a reflection of how little PDS research is done or discussed in the UK. From my experience, by far the most activity and good discussions are going on in the US and in Germany. France is no-where, confirming everyone's suspicion that they still live in a world of their own. They were unlucky (as opposed to the US and UK) in that their language did not become the world language... :-)

There are daily fluctuations in the number of visitors. Typically there are around 30 visitors by working day, and 10 visitors on a weekend day, confirming my suspicious that most of you are abusing your company's Internet access for private matters! :-)

I also noticed that the hits go up the more I post. So this observation is a good incentive for me to post more.

Not much ado about hearing?

There is a discussion going on in the PDS literature on whether deficiencies or malfunctioning in the auditory cortex (responsible for hearing) causes or aggravates stuttering, or whether it hinders therapy. For example, auditory feedback frequency-shifted (FAF) or delayed (DAD) enhance fluency. And in brain imaging studies, the auditory cortex shows a different (lower) activation that for controls. And check out my last post, where I have described my difficulty to realise that my speech has been much more fluent after therapy most times.

These phenomena seem to point to a crucial role for the auditory cortex. But I dont really believe that hearing has much to do with the PDS. In my opinion, the FAF and DAF enhances fluency, because the brain switches to non-automatic speech due to input that sounds unfamiliar. Ingham and others have explained the brain imaging results for the auditory cortex using the concept of efference copy: see here. But, there is certainly truth in the fact that people with PDS often dont notice the progress they have made. I do not believe, that this is a defficiency of the auditory cortex, rather the consequence of a normal functioning. The stuttering is just left out after years of stuttering as a background noise. And the absence of no stuttering sound is just not registered.

I could be wrong and I am open to be converted. This new article out in Neurology Abnormal speech sound representation in persistent developmental stuttering does not really convert me but have a look at their abstract:

OBJECTIVES: To determine whether adults with persistent developmental stuttering (PDS) have auditory perceptual deficits. METHODS: The authors compared the mismatch negativity (MMN) event-related brain potential elicited to simple tone (frequency and duration) and phonetic contrasts in a sample of PDS subjects with that recorded in a sample of paired fluent control subjects. RESULTS: Subjects with developmental stuttering had normal MMN to simple tone contrasts but a significant supratemporal left-lateralized enhancement of this electrophysiologic response to phonetic contrasts. In addition, the enhanced MMN correlated positively with speech disfluency as self-rated by the subjects. CONCLUSIONS: Individuals with persistent developmental stuttering have abnormal permanent traces for speech sounds, and their abnormal speech sound representation may underlie their speech disorder. The link between abnormal speech neural traces of the auditory cortex and speech disfluency supports the relevance of speech perception mechanisms to speech production.

In plain English, the authors have looked at the following phenomena: If you play the same sound to someone several times and then change the sound either for duration, frequency, or related phonemes (the sound units that make up our spoken language), a different brain signal is recorded. This signal is the brain detecting that something has changed. But of course you can only know that something changed if you know what has been before! So the brain must have a representation (or memory) of the preceding sound with which it can compare the current sound. And the authors claim that the signals for complicated sound changes is different to people without PDS. They speculate that the PDS brain does not have good representation of sounds amd is therefore not as efficient in quickly discriminating between more subtle sound changes, and this could encourage development of stuttering.

I had a discussion with Per Alm about their paper, and will post some comments in my next post.

Oblivious to reality

PDS never stops surprising me. It is amazing just how complex humans are despite just being a bunch of cells made out of atoms. :-) Some days ago, I started with a draft for a new post called "Therapy results after 3 weeks". I did talk quite a bit about the therapy in my last posts, and people started asking me about the results. So I wanted to write this, admittedly not very positive statement:

"Last month, I was writing about the Kassel Stuttering Therapy, both from the perspective of a patient and of a researcher trying to improve its efficacy. I also said that I was pretty fluent in the second and third week of the therapy, and was giving talks in front of 50 people or so. So I guess some of you would like to know how I am doing three weeks after therapy. Well, I think it is fair to say that the last three weeks have been a desaster speech-wise. The first week I had several difficult speaking situation asking the tax office to give me back money, being a traffic jam for 3 hours, explaining the dentist in a foreign language, negotiations of a business deal on the phone and so on. So I effectively completely lost it. The real problem is that once I loose it, I have far less control the next time, and I also just forget or postpone practising. Anyway, now I am back practising again and today I started with making short phone calls."

But now compare this statement to a discussion I recently had with my parents:

"Parents: Can I ask you a question? You suddently speak much more fluently. What has happened?
Tom: What do you mean I speak more fluently? I dont think so.
Parents: Yes, you do. What have you done?
Tom: I also did the KST therapy again when I was in Kassel. But I dont think I speak more fluently.
Parents: Come on, Tom. You must be noticing that you have much less blocks and fillers. Why are you lying to us!
Tom: Eeehhh (I start stuttering again) Nnno, not really. I dont really notice this.
Parents: You are strange.."

Somehow those two statements do not really seem to fit well! On the one hand, I talk about the three weeks after being a desaster and they talk about me being much more fluent. Honestly, I did not realise that I had been much more fluent. I think both statements are true. I certainly was very dysfluent in some situations over the three weeks. I know this for sure, because I recorded the phone conversations and listened to them. But one the other hand, I have to believe my parent's statements that I have been much fluent, that is when I was talking to them. So I might well have been more fluent generally, but in very stressful situations dysfluent. The thing that puzzles me is my total ignorance of the fact that I speak more fluently generally. Why dont I realise this? I really must be strange.... :-)