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.