Two breakthrough brain studies!

There is a new article out based on brain imaging work from two top neuroscientists Kate Watkins and Smith at Oxford on the brain of young people: see here and the abstract below:

Using functional and diffusion imaging, we examined brain structure and function in the motor and language areas in a group of young people who stutter. During speech production, irrespective of fluency or auditory feedback, the people who stuttered showed overactivity relative to controls in the anterior insula, cerebellum and midbrain bilaterally and underactivity in the ventral premotor, Rolandic opercular and sensorimotor cortex bilaterally and Heschl's gyrus on the left. These results are consistent with a recent meta-analysis of functional imaging studies in developmental stuttering. Two additional findings emerged from our study. First, we found overactivity in the midbrain, which was at the level of the substantia nigra and extended to the pedunculopontine nucleus, red nucleus and subthalamic nucleus. This overactivity is consistent with suggestions in previous studies of abnormal function of the basal ganglia or excessive dopamine in people who stutter. Second, we found underactivity of the cortical motor and premotor areas associated with articulation and speech production. Analysis of the diffusion data revealed that the integrity of the white matter underlying the underactive areas in ventral premotor cortex was reduced in people who stutter. The white matter tracts in this area via connections with posterior superior temporal and inferior parietal cortex provide a substrate for the integration of articulatory planning and sensory feedback, and via connections with primary motor cortex, a substrate for execution of articulatory movements. Our data support the conclusion that stuttering is a disorder related primarily to disruption in the cortical and subcortical neural systems supporting the selection, initiation and execution of motor sequences necessary for fluent speech production.

Another similar study will come out very soon. Studying and finding similar things. I'll talk about it as soon as it is published.

These two studies are especially significant as they studied young people's brains which should be less affected by years of stuttering. There is now very convincing evidence that brains of people who stutter are structurally different. WE HAVE DIFFERENT BRAINS!

Who says stuttering has no benefit?

There are not only costs to stuttering. Today, I drove down from Princeton to Washington DC on the 95 South. The speed limit is 65mph, which is infinitely slow for a European driver who is used to 90mph. So I was stretching the limits a bit, and much to my surprise a police car gets behind me and makes me tstop. Do you know what I did? I on purpose stuttered as much as I could. Where are you heading to? "Ehhhhh, WWWWWWWasshhh, WWWWaashhhh.." and so on. He was very confused and his face said "Why did I stop this freak?". I got off with a warning. Somehow he didn't want to spend too much time on me.. And who says stuttering has no benefits? :-)

Judy's Online Conference

Here is a link to Judy's online conference 2007. Many different people write articles on many different topics on stuttering: some interesting, some informative, some personal, some the same old stuff, and some misguided! Judge for yourself.

Meeting Jeff Blitz

The rocket scientist, that is myself, met up with Jeff Blitz, the director and writer of Rocket Science in Westwood on Sunday morning for breakfast. Luckily, Jeff also stutters so I had the opportunity to meet my first Hollywood director. He was not accompanied by blonde girls or bodyguards. I met Jeff at the opening of the research center at UCI Medical Center. So if you young, stutter and see no hope for a future career, don't worry: you can still become a Hollywood director, a quantum physicist, a UK pop star (Gareth Gates), a top sprinter (Ben Johnson), guitarist of Wet Wet Wet (Graeme Duffin), professor of comparative literature at Harvard (Marc Shell). I wonder if we also have a famous serial killer or mafia boss in our ranks. Did you make fun of my stuttering? Or if you don't want to be any of the above at least they will meet up with you as you stutter, too!

Jeff is the "older" person on the right with the main cast and the film producer. To be fair, Jeff looks younger in reality, but this is the only picture I could find of him. You definitely need to check out the movie website for previews. The main character is a teenage boy who stutters and joins the debating society. It is good to know that someone who stutters wrote the script and knows what it feels like to stutter. I haven't seen the movie yet, but I am convinced that it is one of the most faithful portrayal of stuttering so far. Jeff spoke about the challenge to present his movies in front of audiences during Q&A sessions. You should also check out his most famous movie, Spellbound, which received many awards including an Oscar nomination for best documentary. And this BBC interview.

The Center for the Medical Treatment of Stuttering (CMTS)

I am currently in Orange County / LA, and I will attend tonight's opening ceremony of The Center For The Medical Treatment of Stuttering at UCI Medical Center, which is headed by Gerald Maguire who is a psychiatrist and the world leading (and only) clinician/researcher on stuttering medication. The center was made possible by a 1 million dollar endowment from Granville Kirkup. The focus of the center is on treating people who stutter using medication, on the research into stuttering medication, and on teaching. They will put out a press release to which I will link.

The center is a really great initiative to explore new avenues in the treatment and understanding of stuttering. The area of stuttering medication is still in its infancy, but shows promises at least for some patients. It's still early days, and some, especially from the traditional stuttering community, are quite skeptical and critical. However, it is also fair to say that most critics do not really know much about neuropharmacology and act out of instinct, and most importantly do not offer effective long-term treatments themselves. I get tens of emails from people who are looking for new avenues as traditional approaches have not helped them a lot. I am not saying stuttering medication is the answer for everyone or a cure for some. But we must explore new approaches.

Jerry has invited me to the opening, and I have been offering him free advice when needed on various issues from statistics, scientific methodology, fundraising to website design. But I'll keep an open mind, and I am not endorsing stuttering medication. I just do not know enough about them, and lack first-person experience. However, I fully endorse the idea that we must spend much more efforts on exploring this new avenue. In the same way, as we should with genetics and brain research into stuttering.

Trying out Medication: Week 1

Here is his experience after one week on Olazapine:

It's a week since I started on the Zyprexa Zydis and the Zantac (generic used). I have been tired, the first 4/5 days were very tiring, it seems better now, less tired. (the 'spaced out' feelings have gone). There has been no noticeably gain in weight, maybe a pound or so, but my weight can fluctuate by 1 or 2 pounds a day anyway.....I have not been able to exercise much this week as I have been so tired, however I am now over this and will exercise from now onwards. I will have a blood test in a couple of weeks to check my levels.

The facial ticks are all but eliminated, I am surprised that this happened so quickly. I feel less/hardly any stress in talking situations and indeed have intentionally put myself into more speaking situations as my confidence has grown. My stuttering has dropped considerably and I am only in week 1 of the treatment. There are hardly any blocks anymore and if it continues at this rate, I will be all but fluent soon - I'd never use the word "cured".

The fact that I am taking the drug may well have given me increased confidence and the upward spiral of confidence has occurred as opposed to the usual downward spiral that we usually experience, so it is self perpetuating. I liken the drugs to a pair of glasses for my eyesight, while I wear the glasses/take the zyprexa it will help my eyesight/speech, however if I take the glasses off/stop the treatment, the symptoms are still there.

Trying out medication: Week 0

I am starting a series on one of your fellow readers who is trying out whether medication is helping his stuttering. (I have edited the report and took out names.)

I am a 39 year old male that has always stuttered. I am married with 3 children, all of which are fluent. I have good and bad days, however over the years it seems to have got worse and I use a good deal of avoidance when entering speaking situations. I suffer mainly from blocks as opposed to repetitions and have major problems with introductions and my name (and other factual things I cannot change).

I have had conventional speech therapy as a young adult and in 2000 I did the McGuire programme. The costal breathing was great, it worked for a while and I was 100% fluent, well I say fluent, thats fluent to people on the outside, as I was thinking/living and indeed breathing stammering 24/7 365 days a year. After the Maguire programme, I got worse and worse as it was hard to go from "fluent" to worse than I was before the programme. I have tried hypotherapy and various CD/MP3's that offer a "cure" - If someone told me that I would be fluent by standing on one leg and chanting, I may have tried that too!!!

I have been doing a good deal of research and after consultation at the stuttering centre at UCI California I decided to take Zyprexa Zydis (olazapine) and Zantac to help offset the weight gain. Pagoclone is still on clinical trials and the drug will not be available until 2010/2011, so I will give the Zyprexa a chance. Prior to going on the drugs, I have intentionally dropped 10lbs in weight (I weigh 200lbs and am 6ft 2" tall) and embarked on a healthy exercise campaign to offset any weight issues that Zyprexa may cause. In addition I had blood tests to get a base line for my fats/lipids/bloodwork.

I took my first medication on Saturday and am now a 300 pound diabetic fluent person!!.....just kidding.....I will be monitoring my weight and will also bloodwork to see if anything changes. The first morning after the drugs, I was very tired, however this is to be expected at the start of taking the drug. As a result, I will make sure that I not be using threshing machinery/flying aeroplanes at 2.30am !!!

If the Zyprexa Zydis does not work or the side effects are too much, I would switch to Abilify which has less side effects but has not been so widely tested for stammering. I will keep a regular update on here so people can see the effects of the drug and also how it affects me in other ways.

Busy

Sorry, I have been busy the last days preparing my US trip. I will visit LA, Orange county, Santa Barbara, San Diego, Boston, Storrs, Princeton, possibly NY on a day trip, and Bethesda near Washinton DC. Let me know if any of you wants to me up.

Re stuttering, I still want to reply to Greg's comments. I also was thinking that instability in speech systems (via genetics or neurological incident) might be a necessary condition but not sufficient condition to develop stuttering. For example, if you have fast-talker genes and you have an unstable speech system, you might develop chronic stuttering, because the system cannot handle the fast speech rate.

Stutter Talk Radio

You should check out this very American but well done and cool talk radio on stuttering: here. Just hit the PLAY button to listen to them:

Greg, Peter and Eric get together and talk about stuttering and life. We have fun, laugh, argue and agree, talk about the stuttering world, music, movies, and our wives and girlfriends. We try and make sense of the whole stuttering thing by talking about it. Tune in and join the conversation!

I hope they will invite me for a guest appearance, though I am a bit scared that I am not doing as well as they in controlling my dysfluencies. ;-)

Does Pagoclone fight the symptoms?

I found this interesting 1998 report on Pagoclone here:

Interneuron Pharmaceuticals, Inc. (NASDAQ: IPIC) today announced results of a Phase 2/3 trial showing that treatment with pagoclone, a novel GABA receptor modulator, statistically significantly reduced the frequency of panic attacks among patients suffering from panic disorder

Putting on the stuttering glasses, the stuttered speech is very often made worse due to the panic that kicks in at blocks. I often feel being out-of-control during my speech, unable to slow down, and then I have even more blocks. According to the study, Pagoclone reduces the frequency of panic attacks, and this effect might very well happen in people who stutter during their speech. They are less likely to get into a panic or the panic will be less severe, thereby giving the person more control of his or her speech, which in turn decreases the probability of blocks.

This would suggest that Pagoclone doesn't act and therfore doesnt tell us anything about stuttering itself (i.e. why do they have many more blocks than fluent speakers?), but reduces the panic secondary symptoms leading to more control and less stuttering.

Stuttering on TV Mission Accomplished

The presentation of stuttering on TV is like the unfortunate Mission Accomplished banner of the Iraq war. The proclaimed victories over stuttering turn out to be just slightly more complicated. But you wouldnt have thought so watching TV shows on CNN, Oprah, or Jauch (a German talk-show). My message: Making a treatment decision based on these shows is foolish. And if you are a parent, plainly irresponsible. Unfortunately, that's exactly how most people choose their treatment. I have to confess that I am also drawn by such TV interviews, and my rational mind needs to fight the emotional manipulation which goes as follows.

a) Create an emotionally painful situation for the audience
- cutie shot of a child that stutters turning in desperation to a female who has this look of "I wish I could help you darling", or
- freak shot of a stutterer with severe symptoms, favourites are head movements, drooling, or 5-second silent (longer is no good as audience might switch to other channel).

b) Get the expert to rationally describe what has just happened. Therefore find an expert that has academic credentials that have vaguely something to do with stuttering, but is very telegenic. If not possible, just label the person "stuttering expert". Experts are often someone the TV crew know, like the sister of the friend of a colleague. If you have to chose between semi-expert but telegenic or "nerdy" real expert, always go for the telegenic person.

c) get the interviewer to engage with the sufferer and show compassion.

d) present a magic unexpected simple and fast solution to relieve the audience from this uncomfortable untenable situation, and explain in black and white. Humans absolutely adore fast, simple and obvious solutions, which obviously do not exist in reality.

e) show child or adult stutterer again but now speaking fluently, talking about how their life has changed. Not very difficult to achieve. Take the most successful patient from a stuttering treatment. Make sure the patients has just finished treatment so to benefit from carry-over fluency. If he still stutters a bit, let him talk for 10 minutes, and only take the 20 seconds where he is fluent! Children are best, because 80% recover anyway. So if you wait a few months, you have a fluent child.

f) now often the sales part kicks in. Where can I get this magic device? Where is this therapy offered? When is the medication available?

g) mention some disclaimer like long-term relapse possible, and my favourite is "talk to your doctor". These words are typically completely ignored as euphoria of the miracle still persists. But legally speaking, you cannot be not sued for your misleading sensational portrayal.

Consequence: The mothers, grandmothers or friends watch the interview, and tell you how stuttering can be cured. You say: But it's not that easy, but they insist and claim you are not doing anything and self-defeating. The fact that you are actually more of an expert than they are is conveniently ignored. After all, it's on TV and CNN and especially Oprah must know better.

Let me say it again: THESE PEOPLE HAVE NO CLUE AT ALL. They are journalists out there to sell a story, and they rely on the experts that they have choosen. I am not saying that some experts are no experts. I would guess 50% are real experts. But even if they actually make subtle statements with disclaimers, the recodings of say 20 minutes are cut down to 2-3 minutes and typically over-simplified.

So if you decide on a treatment, DONT RELY ON THE TV INTERVIEWS. Get in contact with a national stuttering association, and inform yourself. Not only do you make a more informed decision, you also have realistic expectations of your potential progress or that of your son/daughter.

Stuttering sign language

Greg Snyder wrote an interesting article The Existence of Stuttering in Sign Language and other Forms of Expressive Communication: Sufficient Cause for the Emergence of a New Stuttering Paradigm?: see here. Let me post a few extracts, especially as I am sharing some of his thoughts:

While reports of stuttering-like behaviors occurring in sign language have been available for almost 70 years, relatively little attention has been given to its existence and how the existence of stuttered sign may impact our understanding of the stuttering phenomenon. This manuscript provides a brief literature review of stuttered sign and offers a list of potential stuttered sign behaviors. Data is presented suggesting that stuttering is a phenomenon occurring in expressive communication, rather than speech and sign alone. Consequently, it is proposed that the prevailing theoretical constructs fail to account for stuttering in expressive modalities other than speech. It is suggested that the field of speech-language pathology reevaluate and possibly abandon the current pre-paradigmatic views concerning the nature of stuttering so that another perspective can emerge that better accounts for the stuttering phenomenon.

And,

If the data presented in this manuscript does reflect reality, then we are forced to question the belief that stuttering is a speech disorder. On the contrary, the stuttering phenomenon appears to occur in a variety of expressive (communication) modalities. Further, if this suggestion is reality, then stuttering ceases to be a single (speech-related) pathology unto itself. Instead, it is suggested that the observable manifestations of stuttering behaviors are symptomatic responses relative to their corresponding expressive modality. These symptomatic behaviors may be in response to errors in the formulation, processing, and/or execution of expressive output, such as language; it is suggested that these symptomatic behaviors are natural compensatory responses at self correction from errors in processing or initiation at the central level.
In short, if the data and analysis presented in this manuscript do reflect reality, then the traditional views and definitions of stuttering as a speech disorder fail to account for the stuttering phenomenon. Consequently, researchers and clinical scientists may consider abandoning much of the prevailing paradigmatic (i.e., pre-paradigmatic) thought on stuttering, as it can no longer provide a truly scientific and falsifiable theoretical framework capable of accounting for the stuttering phenomenon. If stuttering behaviors are indeed symptomatic responses relative to errors in expressive output, including expressive communication, then a new paradigm will need to emerge to account for this new perceived reality.

Apart from his "making it sound more dramatic and complicated that it really is" style, I roughly agree with Greg, and see two necessary conditions needed for stuttering:
1) glitches in the speech system (leading to an temporary inability to initiate the appropriate speech motor sequence). However I do no agree that stuttering is not a speech disorder, because these glitches are not normal, and are due to defects in the speech system. Stuttering starts inside the brain.
2) compensatory efforts that develop and lead to overt stuttering behaviour and secondary symptoms. I agree that other glitches like in hand signing can lead to similar compensatory efforts, i.e. that these efforts are not specific to stuttering but a generic consequence to certain underperforming systems.

Other blogs on stuttering

Here are my competitors. :-)

I'm Stuck No More
Stuttering Blog
Smithy Strikes Back
1Stutterer
Stuttering Student
Justin's Stuttering Blog
Asia Stuttering Assoc. Blog
Chasing The Fluency God
Pebbles Under The Tongue
Kids Speak Blog
FluencyCast Blog
Closet Stutter Blog
Stuttering-Help Blog (Bud)

Categorising drugs according to impact

Lets put drugs into categories according to their impact, drugs that:
- make stuttering worse for all.
- make stuttering better for all.
- make stuttering worse for some and better for others,
- make stuttering better for some and no impact for others,
- make stuttering worse for some and no impact for others,
- have no impact on stuttering.

I discussed the various systems that drugs could act on: here. It should be possible to systematically go through all drugs, classify them according to the above scheme, look in which brain regions / pathways these drugs are known to act, and then set up a list of the systems involved in stuttering. For example, if a drug has no impact then all the brain regions where this drug act should not be involved in stuttering, and so on. So similar to an fMRI or PET scan, such a study could build up a "drug brain scan" showing the regions of stuttering-relevant activity. Maybe this is practically not feasible, but theoretically it should work!

An all-too-familiar story

I thought I would put this first-person report as a post, because he describes very well what many of us are going through:

I am a 29 year old severe chronic stutterer. After many years of ineffective sessions with various incompetent therapists, trying a couple of those expensive, ludicrous “miracle cure” devices, psychics, witch doctors, benzodiazepines and horrible anti-psychotic meds; I have grown rather hopeless and apathetic towards the idea of my affliction ever significantly improving and completely stopped keeping up with the latest developments and events in the stuttering community.

In a way, losing the hope actually helped me, by making me realize that I am just going to have to live with this condition and making me stop putting off my life until I’m “cured”. I decided to get out there and do the things I want, without worrying what others are going to think of the way I look (talking about the secondaries) and sound.
I now have a job that requires a decent amount of communication and no longer have avoidance issues when it comes to things such as ordering at restaurants, asking for help at a store, getting a drink at a bar, etc. I still have issues with meeting new people and phone conversations with strangers, but I am improving there as well.
Unfortunately, stuttering is still a major hindrance to my social life, especially when it comes to attracting females. It’s definitely wrecking my “game”, which is a major issue, since I would like to meet a nice young lady and start a family within the next few years.
Any way, recently I finally decided to get on the net and catch up on all the latest stuttering-related news and developments. This is how I discovered this very informative blog.
I also learned of Pagoclone and dug up as much info on it as I could find on the web. I am cautiously optimistic and even a little bit excited about it. The prospect of it improving my fluency by even 30% or so is very appealing, because it would make it a lot easier for me to control the secondaries and successfully implement fluency shaping techniques. Because of this, I recently submitted a trials volunteer form, but have not heard any thing back yet.
I am very curious to hear from the people who participated in the previous trials, for the obvious reasons, but also because I am wondering whether it would be a good idea to invest in some Indevus stock right about now. If Pagoclone does get the FDA go-ahead and goes into production, how big is it going to be? Is the market big enough for Indevus to make huge profit off of it? If it going to become the new Ritalin and be overzealously prescribed to every 4 year old who has a minor disfluency? What do you guys ?

TheStutteringBrain in California, Boston &DC

Jerry Maguire, professor at UCLA Irvine and chief investigator of the Pagoclone trials, has invited me to the opening of his research center on October 4th made possible by the generous donation from Granville Kirkup: see here.

So I will be in LA from October 2nd onwards for a week, and then to Boston and possibly DC. So if any of you are from these areas let me know and we can meet up. If you are a millionaire, you can also invite me to stay at your guest house and attend your high-society party. I hope for response from Beverly Hills. :-)

Looking for Pagoclone trial survivors!

If you have participated in the Pagoclone Phase II study and continued its use during the open-label phase, please contact me under t o m DOT w e i d i g a t gmail.com. It would be interesting for me and the other readers to read about your personal experiences. You can make your comments anonymously.

I am actually an actor

Stuttering is very strange for oneself and for others. I have this practical joke I play on non-stutterers and stutterers alike from time to time, along the following line. "Yes, we know you stutter". In a very slow and controlled manner, I look them in the eyes and say fluently "Mmmeee? Nnnoo. Actually I am an actor. I do not stutter, I am just preparing for this movie that I am going to audition in 3 weeks time. I play a person who stutters." Then they are caught off guard, smile nervously and expect me to stutter very soon. But I keep on talking, and talking, and talking fluently! They try everything to put me off-guard but I keep on being fluent... The longer I do it, the more amazed they (and myself, too!) are. And they all wait for me to relieve them "from this nightmare" with a stutter.

I had people starting to believe that I am a true actor! (which of course doesn't surprise me at all given my fantastic looks and charisma! :-) People that know me longer know it's a a bit of a joke, but they are still completely amazed that I have transformed from this "ehhm"- hectic- dysfluent speech person to a confident fluent actor voice... Sometimes they tell me that I stuttered 20 years ago. I am just telling them that I have been acting my whole life... it is boring to be fluent... i just get a kick out of others being embarrassed...

By the way, did I tell you that I do not really stutter. I am doing a PhD in sociology and analyse the impact of blogging on a special interest group...

Subscribe to the Stuttering Brain

You can subscribe to my blog using RSS. Here is what you need to do. This is for the FireFox web browser.
As you read this, look at the address area (htttp://...), and you notice the orange symbol at the end of the address area. Click on the symbol, and you get to a page that allows you to subscribe to the feeds, click "Subscribe Now", and a link bookmark is added to your bookmark bar. If you click it, you can see all the past posts, and you can choose which one you want to read. Once you read one post, the symbol will change next to that post. Good luck! :-)

Where could medication act?

I came up with various systems where a drug could act and improve fluency:

1) the gene expression on genes (partially) causing 2). A drug might inhibit the expression of some genes that make the speech system less stable.

2) the malfunctioning speech system itself. A drug might increase improve a malfunctioning system.

3) systems that decrease the effectiveness of 2) like emotions. A drug might shield the speech system from emotions and work overload, i.e. you can talk as if you are on your own.

4) the primary stuttering behaviour like blocks. A drug might ease blocks and thereby inhibit triggering other stuttering behaviour. You still stutter but softer and less loss of control.

5) the secondary behaviours like loosing eye contact, loosing control, tension, contortions, etc. A drug might inhibit the expression of bad habits or allow a greater control over them.

6) the tertiary behaviours like anxiety, fear, and avoidance. A drug might reduce these, and allow for a better quality of life.

7) the ability of stutterers to successfully implement a behavioural therapy like fluency shaping or dysfluency shaping (van Ripper) short-term and long-term. A drug might make you learn new behaviour faster and more lasting, in fact the drug might be mimicking the brain conditions of the few that are able to follow through and make lasting behavioural change.

Any more fields of attack? Let me know.

Mixing social and natural smile

Let me continue with the social and natural smile analogy: see last post. Often you can see a mixture or a transition between a social and a natural smile. Often, a social smile encourages a natural smile. A natural smile might turn into a social smile, if the joke ends badly. It is as if both systems access your face muscles to different degrees.

I experience similarly in my speech. When I am into the "social" speech like imitating a foreign accent, I am 100% fluent. However, it is not easy to switch immediately from "natural" speech to "social" speech, especially when I stuttered severely before. I need to shut up for 2-3 seconds, "clear my system", start very slowly, and then it usually works. Once I am into it, it's fine.

Interestingly, I just realised that the same is true when I am using a fluency shaping technique! So could we say that these techniques are "social" speech, and is therefore often felt articificial? However, when I am really into the "social" speech, I can somehow modulate it more and bring "myself" (whatever that may mean) more in. So I start with a social smile which goes into a semi or full natural smile...

Keep on smiling :-)

The social smile of stuttering

I spoke to a friend of mine who leads a neuroscience research group, and explained to his astonishment that people with PDS can speak fluently under certain circumstances while singing, imitating a foreign accent, chorus reading, and acting. I also told him about the theory that there are two pathways involved in speaking: one that lets us talk without thinking how we talk, and one that lets us conscuiously modulate our speech. And he mentioned the social vs natural smile phenomena.

People can naturally smile, where they do not control how they move their face muscles, and give a social smile where they decide to smile (even if the joke was bad or they hate their opposite!). A social smile has evolutionary advantages because you can mask your own intentions for the greater good. So let me apply this analogy to stuttering.

When we make a "social" speech, we control how we want to come across. When we make a "natural" speech, we just talk and dont care or are aware of how we speak, it's done automatically. And, in people with PDS, the ability of "natural" speech is sensitive to all sorts of interferences!

Latest from the Nordic Neuropsychology

I insisted until Per Alm gave me a statement of what happened at the symposium!!

At the Nordic Neuropsychology Conference a 3 hour symposium on stuttering was held. The speakers were Katrin Neumann, Gerald Maguire, Hans-Georg Bosshardt, and Per Alm. (Lutz Jäncke was unfortunately unable to attend.) A general conclusion may be that the understanding of stuttering in relation to the functions of the brain is developing relatively fast for the moment. However, it is also becoming increasingly clear that the issues indeed are very complex, and will require a broad range of research approaches for a long time. One aspect that may be mentioned is the progress in brain imaging, which seem to start to shed light on mechanisms for late recovery of stuttering (in teenagers and adults).

I agree with the complexity part. We have hit the complexity wall. Stuttering is a malfunctioning of a highly complex system of interacting modules. I fear a big obstable is that the majority of researchers are intellectually badly equipped to tackle these challenges: we need brains with multi-disciplinary expertise combined with extraordinary lucid conceptualisation ability, rigorous quantitative thinking and an understanding of the nature of complex systems.

I am studying Neuropharmacology

I have decided to learn more about neuropharmacology, and bought the text book The Biochemical Basis of Neuropharmacology by Cooper et al.

Several of my readers are more knowledgeable about stuttering medication, neurotransmitters, and so on. This needs to stop! :-) In a few weeks, I'll be able to make more informed comments.

My current view on neuropharmacology and stuttering is that it might very well help people who stutter but is no cure. The brain chemicals modulate the activity of different brain systems, a bit like different weather impacts a big city in different ways. Dry weather makes traffic jams on highways less likely, but construction work or rush hour still leads to traffic jams, but less severe ones.

No posts

Hi, I havent been posting for a while. I am sorry about that. I'll promise to post soon again.

What should parents do?

I often get asked by parents and relatives what they should do about their stuttering child.

Here is what I tell them:

1) 80% will recover naturally, so with a bit of luck it will go away.

2) go to the speech and language therapist to check whether any other linguistic or neurological issues exist that might create or enhance stuttering. But dont expect them to have a cure.

3) getting the child fluent might be unachievable but keeping the psychological and social impact of stuttering at bay is possible. Talk to the child openly about stuttering with avoiding negatives but also irrealistic positives (stuttering is no handicap at all, it's the others that make it a handicap).Maybe point to other relatives or friends that stutter and tell them that they are successful in life despite their stuttering.

4) get on the Internet and read about stuttering. So you become more knowledgeable and understand better what it feels like to stutter.

5) Re fluency treatment, I find it hard making clear statements. You can try speech exercises and they shouldnt hurt but how much do they help? You could follow a program like Lidcombe or others.

Any more ideas?

Is YouTube making fun of stutterers?

Leys Geddes sent this email around:

Hello, everyone.

As many of you are involved in speaking publicly about stammering, I thought you would be interested to know that recently we complained to You Tube about a number of videos on their site which showed people stammering, or pretending to stammer, which had been classified as Comedy. In response, they said there was no infringement of their codes - so these videos would stay up and would still be described as Comedy.

So we decided to fight back directly and you can now see the result here.



It’s very interesting to note that, over the weekend, the Observer raised a similar issue, in which teachers are calling call for YouTube to ban videos on their site in which children are shown bullying other children.

Anecdote on the pitfalls in research

I havent been posting a lot for the last weeks. I am a bit out of good ideas or the drive to start new ideas! :-)

Here is an anecdote that shows the dangers of accepting every piece of research. I have a excercise bike at home, and it didnt work properly. Sometimes it would just go off, and come back on later. I called the shop and they gave and of course the bike worked!! After they left, it stopped working again! Then it didnt work anymore. I suspected that the bike was fine but that the electric cable had a loose contact that sometimes still worked. So I took the cable to an electronics shop, and asked them to check it. And it worked, so I concluded that it must be the bike. And then it was just standing there for months, as I was just too lazy and stingy to call the shop again. Yesterday, I told my neighbour about my bike, as he is DIY expert in electronics. And it turned out that the cable indeed had a loose contact!!!! We changed the plug and it works perfectly now!!

So what's the lesson? ALWAYS BE SUSPICIOUS OF RESEARCH THAT MIGHT IMPACT YOUR THEORY, AND WAIT FOR 2-3 INDEPENDENT CONFIRMATION. In this case, the third check showed that the cable was a loose contact. I guess the issue was also that it was not always loose but sometimes worked.

Maybe people who stutter have a loose contact that works better at some times than others. And we are misled by some experimental results.

Should placebo be placebo?

I havent been posting for a while. I mentioned the random control trials for Pagaclone to a friend of mine, Gilles (PhD biopsychology), and told him that the trial might not really control for the placebo effect, because Pagaclone is an active compound and does change the brain chemistry. So the patients in the Pagaclone should experience (subtle) changes within themselves, and will know whether they are taking Pagaclone or not, and then they might have a secondary placebo effect: I am taking Pagaclone, so my speech will improve now.

Gilles suggested that the placebo should be a drug similar to Pagaclone, maybe an anti-anxiety drug, because then both groups (the Pagaclone and the control group) will experience a difference, and not know whether they are on Pagaclone or not.

Brainstorming on sub-types

You can group sub-types according to different criteria:
- symptoms (overt, severe, many secondary effects, etc)
- recovered as child (did the person recover as a child or not)
- causes (due to a malfunctioning in the brain processes of speech)
- origin (due to "bad" genetics or neurological incident like infection or accident)
- origin (family history yes or no)
- reaction to treatment
- and more ideas?

Sub-types can be grouped strictly like family history (yes or nor), but others are continuous variables like severity of stuttering. Are there really strict sub-types or are they all just continuous variables?

The number of causal sub-types is the number of intermediate steps to produce continuous speech, because that is the number of times something can go wrong.

CNN on stuttering & Pagaclone

(thx to Dave for the link)

Discussion round at ISA2007

From left to right: myself not looking at the camera, Paul Brocklehurst, Suzana Jelcic (conference organisor), Thomas Kehoe (CasaFuturaTech), and Alan Falck (VoiceAmp, thx for the picture)

Thomas and Alan are selling AAF devices. I tried out them out their AAF device. It forces me to slow down, and this makes me more fluent. I am a bit irritated by the noise in my ear(s). Maybe I should try it out longer.

Thomas Kehoe said that in stuttering there is no placebo based on the result from one study, but I replied that I don't buy it. I rather defend the general principle that there is always a placebo effect, and that the study must be wrong/misleading than give up the general principle. But I also said that the more studies are out, the less I will defend the general principle. But I am pretty confident that there is a placebo effect: we saw it in the Pagaclone study. I will write a more detailed post on the devices.

Subtypes in stuttering

Here are some possible factors that might help divide people who stutter into different sub-types. Here, sub-type is on the cause of stuttering, not on any symptoms like covert vs overt, speech with many blocks vs speech with many fillers/hesitations, etc.

-people who have stuttering genes/gene combinations that cause stuttering vs people that dont.
-people who have stuttering genes/gene combinations that increase probability of having a stutter vs people that dont
-people who have stuttering genes/gene combinations vs people who had a neurological incident
-people who started stuttering at age 3-5 vs people who started stuttering later.
-people who improve/worsen fluency with drug A vs people who are not impacted.
-people who have long-term gains in fluency after therapy vs people who dont.
-people who started stuttering and recovered vs people who never recovered.

Factors that are no relevant in my view to divide into groups with different causes:
-gender
-handedness

Interesting symposium in August

Per Alm has organised a symposium on stuttering in Goteborg: look at Monday morning August 20th in the conference program. Here are the speakers and the title of their talks:

Per Alm, Ph.D. neuropsychology, Lund University, Sweden: Can stuttering be understood from a neuropsychological perspective? A brief overview of research and theories, with special focus on the basal ganglia and the "dual premotor model".

Hans-Georg Bosshardt, Professor, Group for Language and Cognition, Ruhr University Bochum, Germany: Incrementality and modularity in speech production and stuttering: behavioral and electrophysiological data, and discussion of the neurophysiological basis of these processes.

Gerald Maguire, Professor, M.D., Dept. of Psychiatry, University of California, Irvine, USA: Neurochemical and pharmacological experiences from stuttering.

Lutz Jäncke, Professor, Dept. of Neuropsychology, University of Zurich, Switzerland: Neuropsychological research on stuttering.

Katrin Neumann, Ph.D., M.D., Frankfurt University, Germany: Brain imaging of pathology and mechanisms of recovery in stuttering.

Qualifications you need

Here are the qualifications you need to be the first to understand PDS completely. You need to have an good understanding of or need to be:

1) neuroscience.
2) brain scanning techniques.
3) brain pharmacology.
4) statistical methods.
5) genetics.
6) stuttering treatments from patient and therapist perspective.
7) psychology
8) what it feels to be stuttering yourself (ideally, covert, moderate, severe, and recovering)
9) how to network with other researchers
10) getting funds for your research.
11) how to be a very good scientist.
12) high intelligence.
13) good organisational skills.
14) a good orator for conference talks
15) a walking wikepedia and literature review.
16) creative to have good new ideas
17) expertise in audiology.
18) computer programmer.
19) expertise in mathematical modelling

Any more?

Sub-types or not?

Every so often I have a "moment of inspiration". Here is my last one! :-) It's on sub-types in stuttering, and how the power of brain experiments could be improved using knowledge from empirical pharmacology.

1) It is not clear whether there are sub-types or not. However, if sub-types exist, they will significantly complicate any experiment. I mentioned the issue of false negative in my last post, where a compound might not be effective enough in a random control trial because only a minority significantly benefits and the majority not at all. There could be two sub-types, A and B, and the compound is only effective for type A. Or, let's imagine brain scans. And let's assume stuttering is caused by an underactivation of region A or by an underactivation of region B. Of course, in brain research, controls are compared to a mixture of type A and B stutterers. The signal analysis would show an underactivation in both A and B but with only half the strength, and a statistical test might show not statistically significant signals. To conclude, sub-types significantly dampen signals. The same phenomenon could occur in stuttering therapy evaluations.

2) There is somewhat evidence for sub-types. People who stutter seem to react differently to different medication, or drugs like alcohol, dope, or ecstacy. Also, some people seem to react much better to speech therapy that others.

3) There are also theoretical considerations. Speech is a very complicated multi-step and parallel process. However, the effect that characterises stuttering is simple, the absence of an appropriate signal. So many different malfunctions in this complicated process could go wrong, which would lead to the same symptom, the absence of the appropriate signal. Imagine a news speaker reading from a prompter. She will stutter if the prompter gets stuck. But this getting stuck could have several different causes: computer crash or slow-down, the editor did a mistake, and so on. Viewed from this perspective, it would be very surprising if there were no sub-types!

4) There is a chicken and egg problem, because we cannot know whether sub-types exist and identify them because our experiments do not have enough power because we do not separate the sample into different sub-groups!

Here is my solution:
a) put people who stutter in different group according to their reaction to medication or drugs.
b) do brain scans by comparing a sub-group to controls.

This will allow to get much better signals. So again, use empirical pharmacology to form sub-groups and analyse them.

False negatives might be a big problem

I have just changed my view on trials after another email by Willme:

With [Correction Tom: Assuming] several possible (neurotransmitter) causes of stuttering identified, the test results for any one drug applied to a seemingly homogeneous group of stutterers will be diluted. The majority may not respond at all. Morever, even if heterogenity is recognized and a subgroup of stutterers is identified (say responding to BZ's) any one particular BZ, like ativan, may not work for all of them. So the test results could be even further diluted. What this means is that the likelihood of "false negative" test results may be more of a threat than "false positives." With false positives, you take the drug and if it is not efficacious you stop taking it. False negatives imply that a promising drug for a subpopulation of stutterers may fall by the wayside forever.
I hope that there are active research programs out there involving DNA studies to identify the cause(s) of stuttering. I'm quite convinced that genetic markers will need to be found for any substantial further progress.

He is completely right in that a medication that works for a small subgroup will be rejected in a standard random control trial. And everyone thinks it's not working. Different stutterers also react differently to real drugs. Per Alm wrote about this in his PhD thesis. So we need to be able to discriminate between different subgroups, and that's very very difficult because it means we understand stuttering!!! Our best hope is genetics, but we also know that not all stuttering is genetics. So this is not an easy avenue either.

I could even turn the argument around, and say that because no trial has been very successful so far, stuttering must have subtypes.

And then I could argue that drugs that do work, must be acting on secondary symptons and not on primary causes. And this might be the case with Pagaclone.

Check out this NY times story on "On the Horizon, Personalized Depression Drugs." for inspiration on what could happen for stuttering.

Guest-Blogger Willme on ativan (I)

Willme is my next guest blogger and talks about his experiences with legal drug prescriptions and their impact on his stuttering. Interesting thoughts, and he has a PhD in physics like me. :-)

I started stuttering in early childhood. My first experience with speech therapy occurred when I was 13 years old. The therapy involved voluntary repetitions of the first syllable of each word uttered and the application of this technique in a public context. This approach didn’t work for me. I basically refused to practice this technique in public—perhaps I was too embarrassed, self conscious, etc.
When I started puberty very late at the age of around 17 my fluency substantially improved. I joined the National Forensics Society and on the debate team and engaged in forensic speaking. By the time I entered the 12th grade, my disfluency had returned. Maybe temporary changes in brain chemistry at the start of puberty offered a temporary “cure?
My next speech therapy occurred in my later 20’s after I completed graduate school. It was a group therapy setting with four other males in their late teens and early 20’s. There did not seem to be any particular therapy techniques involved other than making eye contact and the admonition to “just stop it.” Well, strange as it seems, it worked for me. Within two weeks, I became, as far as I could tell, perfectly fluent within that group context. So I called it the “power of positive thinking” (POPT) or the “mind over matter” (MOM) approach. For the next couple of months before I left the group, the POPT/MOM approach did not work for the four other people.
I then started four years of psychotherapy (twice a week) and began teaching in a graduate program at a university. The POPT/MOM approach tided me over but I found that for anxiety inducing situations (speaking before a class or at a conference) I had to expend a huge amount of energy preparing myself, both content-wise and emotionally (psyching myself up?). Also, during psychotherapy, I found that I would be disfluent when discussing emotion laden subjects.
After years of teaching and research, I moved to a career in consulting. Public presentations were fewer than in the teaching career but the POPT/MOM approach still worked (still requiring a huge expenditure of energy). A few years into this period I began to take ativan (Lorazepam) for anxiety and eventually found that at a 2 mg dosage virtually eliminated disfluency. And there was no need for extensive content/mental preparation before presentations. I would merely engage in “normal” preparation, take 2 mg of ativan about a half hour before the presentation (on an empty stomach) and, miraculously, I was perfectly normal.
My last eight years I returned to a career in university teaching and continued with the ativan therapy. I would teach two graduate courses per term and present papers at approximately 4-5 conferences per year. The courses might be scheduled say for Monday and Thursday between 6pm-9pm and the 2 mg of ativan tided me over for the three hours. So my intake of ativan was sporadic rather than regular, which is important because ativan can be addictive, its effect lessens if used regularly, and, hence, you may require larger dosages. I would certainly not recommend the use of ativan to anyone who is an addictive personality.
...to be continued...

NOTE: PLEASE CONSULT WITH A DOCTOR BEFORE TAKING ANY MEDICATION TO TREAT STUTTERING!

Guest-Blogger Willme on why ativan might work for him (II)

Let’s try to understand what’s happening from the research perspective. Given that ativan 2mg has worked so well for me, I am puzzled that no one else among the estimated 3,000,000 stutterers in this country has discovered its efficacy. Am I the only one for whom this drug therapy works? If it works for other stutterers, for what fraction of them is ativan effective? Is what I’m experiencing a placebo effect whereby I go from some level of disfluency to virtually a zero score on the stuttering severity instrument?
Ativan (technically known as lorazepam) is a benzodiazepine (BZ), which binds to the BZ receptors in the brain. BZ receptors seem to be coupled to receptors for the inhibitory neurotransmitter gamma amino butyric acid (GABA), which is the most prevalent neurotransmitter in the brain. BZ and GABA receptors coexist together in an interactive complex known as GABA-BZ (Receptors, Restak, R.M., Bantam Books, 1994, pp 166-167). BZ’s (the most notorious of which is valium), inhibit anxiety just like GABA. So ativan is regarded as a GABA agonist since it binds to GABA-BZ receptors and when it does neurons are less likely to discharge. Correlates of anxiety involve excitation (more rapid firing of neurons) and BZ’s reduce this excitation. By the way, previous studies have shown the ineffectiveness of BZ’s with respect to improving fluency (The pharmacology of stuttering: a critical review, Am Journal Psychiatry. 1991 Oct; 148(10):1309-16.Brady JP). One of the studies cited in this review that I acquired used valium (diazepam) at 5 mg dosages. I don’t know what the conversion over to ativan dosages is.
Now most of you have heard of pagaclone, currently in phase III trials as a palliative for stuttering. Pagaclone is identified as a partial GABA agonist, the “partial” referring to its lack of sedative and withdrawal effects. It too binds to the BZ receptors. The most recent press release of Indevus Pharmaceuticals indicates that phase II trials have been a roaring success in reducing disfluency. The way that pagaclone was identified as a potential palliative for stuttering was that in previous trials testing it as an anti-anxiety agent there happened to be at least one stutterer in the test group and he (she, they) reported a marked improvement in fluency levels. So to answer one of my questions above, there are at least two of us who recognize that GABA agonists/partial agonists may greatly improve fluency. To my knowledge, pagaclone was never released as a prescription drug to treat anxiety (in spite of claimed success in the anti-anxiety trials), so the possibility does not exist for our buying it and using it off label for disfluency.
A second major research direction in the current pharmacological treatment of stuttering. involves basal ganglia/dopamine system (BG/DS) theories. This line of research seems to be mutually exclusive from the GABA/pagaclone efforts or, at least, researchers have not yet found any connection between them. The BG/DS theories revolve around malfunctions in the basal ganglia very deep in the brain and the presumed production of too much dopamine, which is another neurotransmitter. Dopamine is associated with addictive illegal drugs, Parkinson’s disease (a lack of dopamine), and reward systems. Risperidone is a dopamine antagonist and has been claimed to improve stuttering in clinical trials (for a good review,see Stuttering and the Basal Ganglia Circuits: A Critical Review of Possible Relations, Alm, P. in Journal of Communication Disorders 37, 2004, pp 325-369). This review article also cites studies in which stimulants were used to increase dopamine resulting in improved fluency. So the author of this article concludes that there may be two types of stutterers, ones who improve on dopamine antagonists and others who become more fluent on dopamine stimulants.
Incidentally, I’ve tried the antianxiety drug Buspar which binds to dopamine receptors ( a moderate affinity for D2-dopamine receptors) and reduces the influence of dopamine (a dopamine antagonist?). I found it has no effect on either my fluency or my anxiety. Fifteen minutes after ingesting the drug I get a buzz in the brain and feel spacey for about half an hour. And even more incidentally, I’ve tried a variety of antidepressants (serotonin uptake inhibitors only) and these have had no effect on me whatsoever.
So the question is: Are there indeed different subclasses of stutterers who respond to different treatments—those with not enough GABA, those with too much dopamine, those with not enough dopamine, etc. Having trained as a scientist, I would prefer to follow the “law of parsimony,” and try to explain a phenomenon with a single theory rather than a collection of theories. But nature may not be so neat. If the subclasses of stutterers multiply, then it may be very difficult to get positive results from clinical trials. For example, if only some fraction, F, of stutterers respond to pagaclone, and that fraction F is too small (say less than 10%), then the trials may not be able to identify significant differences between the group receiving the drug and the one receiving a placebo. In addition, if the fraction is too small, the drug company may feel it not worthwhile to market the drug.
To answer the question as to whether the fantastic results that I experience with ativan 2mg is a placebo effect, I have some anecdotal evidence to offer. Several times before teaching my 3 hour graduate class I had forgotten to take the ativan and found at the start of class that I was disfluent. After several minutes of this I realized what the problem was. The second bit of evidence occurred at a conference in Texas at which I was giving a presentation. The presentation was scheduled just after lunch and prior to the presentation I had a Tex-Mex meal which impeded the ingestion of the ativan that I did take after the meal but before the presentation. Once again—a lack of fluency. While this evidence isn’t as good as a controlled double blind experiment, at least I’m convinced that we don’t have a placebo effect in play here.
Given my experience, you can understand my enthusiasm for the pagaclone trials. Like most of you I’m impatient to try it, but I think it will be more than a year before it comes on market, if indeed it reaches market. Then we’ll have to worry about price gouging by the pharmaceutical industry.

NOTE: PLEASE CONSULT WITH A DOCTOR BEFORE TAKING ANY MEDICATION TO TREAT STUTTERING!

Pagaclone open-label release misleading??

Here is what Indevus wrote about the new open-label results for Pagaclone:

The open label data demonstrated an improvement in nearly all efficacy measures compared to baseline that was at least double the magnitude seen in the initial 8 weeks of double-blind treatment. During the 8-week, double-blind portion of the study, patients who were randomized to placebo experienced a mean reduction in the percentage of syllables stuttered of 5%. After three months in the open label portion of the study, these same patients experienced a 31% mean reduction. These open label gains lagged slightly the gains made by patients originally randomized to 8 weeks of active pagoclone (5 months total exposure). For those patients randomized to pagoclone in the double- blind phase, the mean reduction in percent syllables stuttered was 18%, while in the open label phase, the mean reduction was 40%.

Similarly, data for the Clinician's Global Impression of Improvement (CGI- I) showed considerable gains during the three months of open label treatment........

Superficially good results. But I am a bit suspicious due to this relevant quote later in the press release:

More than 70% of the 119 patients who entered the open label phase of the EXPRESS trial were included in the three month open label data being presented at NCDEU.

In effect, 30% of the people decided to discontinue the use of Pagaclone. I would not be surprised that only the people who had a positive effect continued, so it is not surprising at all that there was at "least double the magnitude seen in the initial 8 weeks of double-blind treatment"? And most importantly, should you not actually evaluate all the patients after the 3-month open label, even those that did not take part to see the overall efficacy of Pagaclone?? Their statement of improvements is a bit misleading, because they only mention much later that only 70% took the open-label invitation up.

New Pagaclone results are out!!

Indevus today announced some further results of the Phase II pagoclone trial, along with some results from the 3-month open label period (after the 8-week initial double-blind trial), see here. More later.

Be a guest blogger!

This is an invitation to all the readers of TheStutteringBrain to be a guest blogger. If you feel you have an interesting idea, want to raise an issue, discuss a research paper or had an interesting experience, please email me at tom DOT weidig AT gmail. I only require that the topic of your post is vaguely related to the science/research theme of my blog, namely to Sharing with you the on-going revolution in the understanding of Persistent Developmental Stuttering.

Sandra Merlo as guest blogger (I)

I am happy to present Sandra Merlo from Brasil as The Stuttering Brain's first guest blogger. It is her talk at the ISA conference on Personal and professional experiences:

My stuttering started between 3 and 4 years old. It was near when my brother was born, so my parents concluded “I was jealousy and I wanted attention”. Some years later, my brother and a cousin also started stuttering and my family concluded they were imitating me. The fact was that stuttering affected several members of my family. From this fact, I had my first wrong lesson: stuttering could be learnt from imitation.

I remember that when I was 6, I already had well established strategies of avoidance (speaking less, changing words, changing phrases, not speaking with some people and so on). Even so, I could not hide stuttering all the time no matter how hard I tried. But my mother repeatedly said I was not trying hard enough, because if I really wanted I would get it. The fact was that I could not control stuttering. From this fact, I had my second wrong lesson: I did not have enought will-power.

When I was a child, I also realized that my stuttering was better in some days, with some people and talking about some topics. The fact was that I realized my stuttering had an oscillation. From this fact, I had my third and fourth wrong lessons: stuttering should be psychological and if sometimes I was better, if I tried hard enough, I could always be better.

When I was a child, I also noticed my family, teachers and friends almost never talked about my stuttering. The fact was that there was a great silence about stuttering. From this fact, I had my fifth wrong lesson: stuttering should be a so shameful thing since no one talked about it.

When I was 10, my Portuguese teacher said I had to go to a “speech-language pathologist” (SLP). I had never heard this expression before. I did not know what a SLP did. I told my mother I would like to go to a SLP, but she remembered me my pediatrician has already explained that I just had to repeat fluently what I said stuttering. According to my pediatrician, if I did this, I would be cured from stuttering. The fact was that I had wrong professional advice. From this fact, I had my sixth wrong lesson: I did not need a therapy because I could overcome stuttering all by myself.

When I was 14, I was in a great suffering, suffering entirely alone, feeling very imcompetent and with absolutely no hope. So, I decided to commit suicide.

(To be continued…)

Sandra Merlo as guest blogger (II)

But then, my English teacher realized I needed help and, for one year, he constantly talked about my qualities and my future in our classes. So when I was 15, I decided to be a SLP, because I desperately needed to understand the world I was living in.

I was admited at University of São Paulo, one of the best universities in Brazil. For the first time in my life, I had a positive consequence from my stuttering: my personal experiences with stuttering provided me with a great background to understand scientific knowledge in my years of SLP School (1997-2001). Scientific knowledge quickly made sense. At the same time, I did speech and psychological therapies.

Afterwards, I was admited to State University of Campinas, also one of the best universities in Brazil. I got a Master’s Degree of Linguistics (2003-2006), studying periodic cycles of hesitation phenomena in non-stuttering subjects. At this moment, I am attending a Doctoral Degree of Linguistics at the same university and I am studying periodic cycles of pause and the relation between hesitation phenomena and pause in non-stuttering subjects.

I have also worked at the clinical division of a SLP company, giving assistance just to patients with stuttering. My patients displayed two major characteristics: they usually needed differential diagnosis (especially regarding to cluttering, motor and vocal tics, dystonia, obsessive-compulsive disorder and attention deficit hiperactivity disorder) and they have usually done several previous therapies without success.

Last year, I got involved in Brazilian Fluency Institute, a non-profit association devoted to fluency and its disorders (stuttering, tachylalia and cluttering). Some of our actions include: the organization of the Brazilian campaign of International Stuttering Awareness Day, a great participation in the media to talk about stuttering, information and advice about fluency and its disorders, legal advices about stuttering and supervision on research.

So, now, after SLP School, Linguistics School, clinical practice and Brazilian Fluency Institute, I think I have more reasonable answers for my childhood wrong lessons.

(To be continued…)

Sandra Mello as guest blogger (III)

When I was a child I used to think stuttering could be learnt from imitation, but scientific knowledge presents evidence that, instead, stuttering may be caused by an hereditary factor or by a brain lesion (Alm, 2004; Drayna et al, 1999; Ludlow & Loucks, 2003).

When I was a child I also used to think stuttering should be the result of psychological problems, but scientific knowledge offers evidence that stuttering may be the result of basal ganglia (BG) disfunction (Alm, 2004, 2005; Ludlow & Loucks, 2003; Molt, 1999). In this case, BG would sometimes fail to generate commands to finish some sounds or syllables. This is exactly what I feel in my speech: I feel I start saying a sound/syllable and get stuck on it. This is also the way my patients usually describe their stuttering.

When I was a child I realized stuttering level had an oscillation and I thought I could control this. I did not know waxing and waning periods are intrinsic to the BG disorders and that this cannot be controled. I used to think that if I tried hard enough, I could always be with a good fluency level.

When I was a child I also used to think I did not have enought will-power, because I could not always hide my suttering. Scientific knowledge offers evidence that BG functioning is not under voluntary control. So, as a consequence, stuttering is not under our voluntary control.

If psychological problems do not cause suttering, what is the role of emotions in stuttering? I think Per Alm (2004) hits the nail on the head when he says the level of freezing response can explain emotional influences on suttering. The freezing responde occurs when the person antecipates an unpleasant situation with regard to stuttering that is going to happen and he/she does not know the best way to act and he/she does not decide fight or flight.

When I was a child I also used to think stuttering should be a so shameful thing since no one talked about it. In Brazilian society, stuttering is understood as a minor problem of minor people. I think because of this very few people and very few professionals are interested on stuttering.

Finally, when I was a child I also used to think I did not need treatment because I should be able to overcome stuttering all by myself. But this is really not the case: according to my experiences as a PWS and as a SLP, professional help is amost always necessary. Nowadays, we have at least three ways of professional help: speech therapy, pharmacological therapy and/or psychological therapy.

I used to blame myself for my stuttering, I used to blame my parents for not conducting me to a specialized treatment when I was a child, I used to blame my pediatrician for wrong professional advice, I used to blame my destiny… But, when I was 15 and I decided to be a SLP, I realized this was not a good way. I realized I could try to do something useful from my experiences: I could try to understand stuttering, I could try to improve my speech and I could try to help other people. At least try.

What is a cure?

Here is my cure level ranking.

Cure Level 4: relatively fluent but massive avoidance.
Cure Level 3: noticeable but not severe disfluency with only minor avoidance.
Cure Level 2: relatively fluent and minor avoidance.
Cure Level 1: no stuttering signs and no avoidance.
Cure Level 0: fluent without thinking and no tendency for relapse.

My statements for the day:

1) I give preference to less avoidance at the cost of less fluency.
2) Nearly everyone can be at level 1, 2 and 3 after therapy.
3) Most slowly fall back to level 3 and 4 sometime after therapy.
4) No-one ever reaches Level 0 fully.
5) Level 2 is realistic with hard work, and patience.
6) Depending on the severity, some people can reach a higher level more easily.

New evidence for basal ganglia theory?

Here is a new article published in Brain & Language on new evidence that the basal ganglia is involved in stuttering. Giraud AL, Neumann K, et al. report:

This fMRI study reports a correlation between severity of stuttering and activity in the basal ganglia and shows that this activity is modified by fluency shaping therapy through long-term therapy effects that reflect speech production improvement. A model of dysfunction in stuttering and possible repair modes is proposed that accommodates the data presented here and observations previously made by us and by others.

I write more once I have a copy for the article.

Discussing the Lidcombe RCT

Ora writes:

I've just read your September 2005 letter to the BMJ "The statistical fluctuation in the natural recovery rate between control and treatment group dilutes their results. The statistical fluctuation in the natural recovery rate between control and treatment group dilutes their results" You wrote: I find a 10% probability that a "minimum worthwhile difference between the two arms set at 1.0% syllables stuttered" occurs due to statistical fluctuation and not due to treatment effect. The standard aims for a less than 5% chance that the observed results occur by chance (usually expressed as p<.05), whereas you're observing that this trial achieves only 10% (p<.10). Is that what you're saying? If so, 90% is obviously not as powerful a result as 95%, but it's not worthless either.

I show that two control groups (i.e. I assume no treatment effect) have a worthwhile difference in 10% of all cases, because the natural recovery rate causes the groups to start at a different baseline (they have a different percentage of natural recovers by chance) (This effect gets smaller with increasing sample size). Then I argue: If with no treatment effect, I have a 10% chance of seeing an effect, then something is wrong because I should expect that in 0% of the cases there is an effect because both groups receive no treatment. So their p-value (which they claim less than p<0.01) MUST BE wrong and higher, because the t-test assumes that they are the same. So their statistics is wrong, and they must re-do their stats. What exactly the value is is not easy to compute.

Possibly instead of choosing an effect size (1.0% difference in syllables stuttered) that allowed them to claim p<.10, they should have claimed a smaller effect size (for example, 0.5% difference in syllables stuttered) that would have supported the stronger claim of p<.05.

What you are doing is shifting the criteria to get a result! See my arguments above, we need a strong signal to be sure that no other systematic effect can destroy it.

Though I don't fully understand your argument in your Sept 2005 letter, I would agree if you're merely saying that their results may not be as strong as they're suggesting. But on the other hand it seems to me that your claim that "the random control trial did not show efficacy despite their claims" is also too strong; 90% may not be 95%, but a 90% number is still strongly suggestive.

I am saying that the p-value is much higher, but I do not know how much higher.

However, there is at least one more crucial flaw in the study that I haven't talked about in the letter but I did in my talk which supports my claim that they have not convincingly shown efficacy. They only observe the kids for 9 months. Let's assume that the only thing Lidcombe does is to accelerate the recovery of those kids that would have recovered anyway, then I see a treatment effect over the short-term. Here is how it works. Lets assume at the start 100% of the kids stutter, and after 2 years only 20% of the kids stutter, those that do not recover naturally. I also assume that 40% recover naturally per year, so I have 40% first year, 40% second year, and 20% don't recover. If I run the experiment for one year. Then in the control group only 40% recover, but in the treatment group 80% will recover (remember I assume that Lidcombe makes the kids who recover naturally recover faster). And so I have a 40% higher recovery in the treatment group!!! But if I wait for one more year, the control group will have the other 40% kids recover naturally, and then there is NO difference any more between the two groups!!! So they need a longer observation period to control for this effect! Another aspect might be to look for relapses of kids...

Mark Onslow and Lidcombe at ISA

At ISA, I attended Mark Onslow's workshop on the Lidcombe program. He didnt seem to be very pleased when I told him during the workshop that his random control trial is flawed. The day before, I had given a talk (which Mark did not attend, I think) on why the random control trial did not show efficacy despite their claims. Sue Block was not too pleased, and said that random control trials are widely used in all kinds of areas. Of course, this is the typical response without addressing my arguments. Why can no-one say: Tom, I have listened to your arguments. I don't agree with your argument on slide 10, because of X and Y. That's why you are wrong. No, everyone says but RCTs are widely used, or the RCT's statistics have been computed by a statistician. Which kind of scientific debate is this??? Anyway, I met Sue Block later at the B&withnoB, and we had a more constructive debate.

Several people approached me regarding my talk or even congratulated me for standing up against Lidcombe. I just want to emphasise that I am not really against Lidcombe, just against their claim that they have shown efficacy with an RCT. I am not an ideologue who feels a strong urge to defend his/her view of the world. Here are my thoughts:

1) I have been to the workshop, and overall the program seems to make sense and I dont think it will harm the children at the very least. In fact, it does encourage good parent-child interaction, which should be beneficial anyway. So it might well prevent greater behavioural, social and psychological effects from developing.

2) What I do criticise is that Mark Onslow claims that research has shown efficacy. However, as I said before, they have proven anything. In fact, during the workshop he himself showed some long-term data that suggests that only 84% of the children recover, which is close to natural recovery.

3) My guess is that Lidcombe might well help kids to recover faster that would have recovered anyway, might well ease tension between kid and parents (the therapist acting as supper-nanny), and for the non-recovers reduce some secondary effects, BUT I doubt very much that it makes the kids fluent that would not have recovered anyway. To do this, the program is not interventionist enough and one needs to do more active speech work.

4) If I had a stuttering child and the choice of doing nothing or doing Lidcombe, I would certainly do Lidcombe with them.

5) I get the feeling Mark does not really know how to handle my statistical arguments, but his statistician should have: Mark Jones. He has never properly addressed my issues I have raised by replying to my email or my rapid response in the British Medical Journal.

6) Lidcombe might well have an effect but on a behavioural (less severe secondary effects like grimaces or strong blocks) and psychological (avoidance and shame) level, which is much more difficult (if not impossible) to capture in a trial.

ISA: Too expensive at average quality

Despite the beautiful site, I found the congress quite expensive, especially as I had to pay it all by myself. And in general I found Cavtat and Dubrovnik quite expensive for the quality offered. I spent several holidays in Italy, and I have to say that the food in Italy is much better and similar prices. The people are far more friendly and you are less treated like a walking euro/dollar symbol.

For example, the gala dinner food was not very good. First of all, they only served champagne at the reception on the top terrace, not even water or orange juice. When I asked for orange juice, the waiter said: No. Everywhere else, they would have organised something, but not here. Big Minus. The buffet food was mass production. They even managed to have factory cakes as dessert: you know the one you can buy in the supermarket next door in boxes of 100 or 200! And the fish risotto was far too salted.

Next comes my hotel room. I booked through the conference organiser's recommended travel agent, because I assumed that they would make sure that the deals are fair. So I paid 70 Euros for a very very simple room in a flat complex 5 minutes from Hotel Croatia, and with breakfast at Hotel Croatia. As I stayed one day longer, I was curious how much the room in the neighbouring bed and breakfast would cost. I paid 20 Euros!!! So in fact they made at least 40 Euros per day. This was a complete rip-off, and I think it was irresponsible of the conference organisers not to check whether the deals offered by the agents were fair!!!

Then the day trip to Montenegro cost 90 Euro. I didn't go, because I was still upset by the way they "stole" 5 times 40 Euros from me. 90 Euro per person for a day trip is ridiculous. The bus costs at most 15 Euros per person, then lunch 20 Euros, and the guide 5 Euros, so in total 40 Euros at most! Again every single person was ripped off by 50 Euros!! Again, I blame the conference organisers for not making sure the deal very fair.

I did tell one of the organisers and someone from ISA that I found the price far too high for the services offered. And I think it is especially unfair for the many visitors from poorer countries. OK, I shut up now... :-)

A beautiful site for the ISA congress

ISA is the umbrella organisation of the national stuttering associations, and has a congress every four years. The last congress was is Perth (Australia). This year's congress was in Croatia in Cavtat near Dubrovnik. The conference itself was held in Hotel Croatia which is beautifully set on a hill next to the coast. The first picture shows the hotel's terrace where conference participants sat during breaks. The great thing was that they had a free wireless network! The next picture shows the nice hotel beach. I spent two days there. There was no sand, but it was OK. I also went swimming there.
The most useful room in the hotel was the disco/bar Posseidon in the cellar. The design is all Austin Power style, and a big dance floor in the middle. It was open every day, and often people from the conference would get together there. I even managed to convince Velda Osborne, Chair of the BSA and member of the Older Generation, to join in after the gala dinner. The next day she blamed me that I had been a bad corrupting influence on her, and that I "made her" stay at the bar until 3 o'clock in the morning. When she went up to the reception to get a taxi back to her hotel, the porter said "But Madam, it is 3 o'clock in morning, there are no taxi." And then I think he drove her back...Picture are from the net. If someone has better pictures, pls let me know!

Summary of ISA

Sorry I havent posted for a week. I needed to recover from the intense ISA conference in Dubrovnik! :-)

I really should have posted real-time from the conference, but unfortunately I didnt. As soon as I get too many different inputs, my focus gets hijacked.

Here are the topics that I will talk about:

0) A beautiful site for ISA

1) The high costs of the conference

2) Tom and Lidcombe.

3) AAF Devices and their usefulness.

4) Jaik at ISA.

5) People from all around the world.

Back from ISA / Live feeds

I am back from the ISA Congress from Dubrovnik (Croatia). I had a great time, and I will write more soon.

There is/was a live feed for the ISA Congress: here. I am not sure whether there are recordings of the key note speeches. If you know more, pls let me know.

Sorry, I wanted to post this information much earlier. By the way, the live feeds were done by Manfred. (I forgot his family name). Many thanks to him. This allowed people from around the world to be part of the ISA congress.

ISA(II)

Tim Saltuklaroglu spoke about the impact of stuttering on the physiological state of the listener. He showed that the listener has a lower heart rate and more blinking. Clearly, the listener reacts. There were many questions.

At the end, Illia and Natalia Rasskazova showed their software NEODIALOG that trains effective communication by measuring intonation.

More soon, my battery is nearly empty.

ISA live (I)

Right now, I am in a talk at the ISA conference. Already after the first slide, I fundamentally disagree with the lecturer! So let me talk about the research session that I chaired this morning.

Patrick Kelly talked about his experience as a therapist for a rural area in Ireland. He has worked there for more than 10 years and sent out a questionnaire to all his past children that he treated. He reports are very high recovery from stuttering; I think 44 out of 46.

Then Jelena Tadic showed evidence that many children who stutter also have articulatory problems. However, her sample was quite small, less than 20. So I am a bit skeptical.

Then Soster claimed that the voice of people who stutter shows difference to normal speaker's voice. I am a bit skeptical, and suggested that she should do the reverse test, i.e. is it possible to identify stutterers by only listening to their voices?

Off to the ISA conference

I am off to the ISA (International Stuttering Association) conference in Dubrovnik (Croatia). I might be blogging from there, depending on the availability of Internet Access.

Too much blogging..

Too much blogging about stuttering is bad for you. Here is what happened to The Stuttering Student. :-) Funnily enough, when I met him in San Diego, he came across as rather calm and a bit shy!!!

Competition from junior stuttering brains

Oh my god, the competition is getting younger: The Kids Speak Blog.

Monkeys, Hands, and speech

Have a look at this BBC science article: here:

They analysed the way two types of apes that are closely related to humans use hand and limb gestures to communicate. The scientists found that apes used gestures more flexibly than the way they used facial and vocal expressions. They say the findings support the theory that human language developed through the use of hand gestures.

The most appealing argument for me is that for most people the right hand is the dominant hand, which is controlled by the left-side brain. And speech and language is located only in the left-side brain. This is more than a coincidence.

I am talking about this connection, because people who stutter have subtle dual tasks defficiencies with hand or finger movements: see previous post. Maybe this is all related?