Tuesday, January 31, 2006
I would guess that the distinction becomes clearer the more demanding the speaking situation: from reading to talking while doing other tasks.
I believe that you can distinguish the "recovered stutterers" vs "normal" people quite accurately. I often hear "recovered stutterers" who are fluent and communicate well, but still you can sense they struggle more and speak more controlled, less spontaneous and ironically too fluent without natural disfluencies!! :-)
The interesting question is whether you can distinguish between people who stuttered as children and those you didn't stutter as children. Is it possible to detect a difference? I guess that it might be possible but only by severely stressing their brains... If it is not possible, either stuttering is just a learned behaviour or the brain completely compensates for a weakness.
Saturday, January 28, 2006
So let me ask the people with PDS the following question. Contrary to what I have been saying there is a cure (but just for this paragraph and then there is no cure. OK? :-)
The cure is quite simple: you need to do a daily exercise and then you are completely fluent for the rest of the day.
If the exercise takes 5 minutes, would you do it?
If the exercise takes 15 minutes, would you do it?
If the exercise takes 30 minutes, would you do it?
If the exercise takes 1 hour, would you do it?
If the exercise takes 2 hours, would you do it?
What is your tolerance? I think mine is at 30 minutes. And 1 hour if I can skip days and only use it if I really need it.
So now there is no cure. OK? But now I am the devil, but just for this paragraph, OK? :-)
So I am Devil Tom, and I have real superpowers. Do you want to make a deal with the devil?
Would you like to exchange your stuttering for your little finger? for a leg? for being blind on one eye? for being deaf? for being less intelligent (assuming you are intelligent)? for being ugly and oversized (assuming you are not)? for the house that you own? for your wife? (be honest with yourself! but dont tell her)
But unfortunately, I am not a devil.... at least not with superpowers. ;-)
Friday, January 27, 2006
So often people say I am cured because I did A and B which followed from my theory of stuttering, but this is a logical fallacy. Other theories might also get to A and B!!!
Thursday, January 26, 2006
Wednesday, January 25, 2006
1) I am a stutterer. What do you do?
2) I stutter, but I am not the only one.
3) I live with a stutter but not with my parents anymore!
4) I st--- you know what I mean...
5) I am not quite as fluent as you, my dear.
6) You are so beautiful you make me stutter.
7) I was part of the Monster study.
8) I was a method actor for a Hollywood movie on stuttering but they took Tom and I kept stuttering.
9) My mother gave me gene Xi-362 - bitch.
10) I am the re-incarnation of a recovering stutterer's soul from the psychodelic 60s when he still stuttered!
Let me know if you have more.
Monday, January 23, 2006
These expressions might be OK for superficial use, but are quite sloppy and inaccurate expressions, because
1) non-pws stutter occasionally,
2) pws are sometimes not stuttering,
3) some pws rarely stutter but avoid,
4) most children who stutter do not become pws,
5) and people having had a stroke stutter but differently!
The term "stuttering" is also quite ambiguous as it refers both to
1) the main symptom of the disorder i.e. "dysfluent speech" and
2) the disorder itself,
leading to endless confusions.
I think "stuttering" is best left to mean the main symptom of the disorder i.e. "dysfluent speech" plus possibly secondary symptoms, and the disorder should be called "persistent developmental stuttering" (PDS), which makes the distinction between two related but different disorders non-persistent stuttering (childhood stuttering) and non-developmental stuttering (due to a neurological incident like a stroke). And then the "pws" are people with PDS, or possibly having or suffering from PDS. More on this post on my blog.
Per Alm mentioned two other expressions to me: dsyphemia, and gluency:
"I think the old concepts of "dysphemia" and Van Riper's "gluency" are relevant here – see my thesis page 22. However, I have no clear opinion about what terminology to use. For example, I do not think dysphemia is a good word but I think we would need a word for that concept".And he betrays me by saying that
"For example, I'm not using the concept PDS very often because I think there is no sharp division between PDS and "acquired stuttering", with onset after for example head injury. I think the number of neurological lesions in "developmental" stuttering has been underestimated. "
Saturday, January 21, 2006
An automatic habit is a process that runs independently of an executive order by the person. You might be choking when swallowing a pill, getting nervous when the phone rings, looking down when you have a block, word substitution when you cannot say a word. This process is more or less automatised, and cannot be controlled at all or only with outmost focus, attentation and energy. You can force yourself to look into someone's eyes while blocking, but it is very hard if you have always looked down. Such habits are really programmed in your brain, most likely in the amygdala that says in "Situation X -> do Y without asking for permission by the cortex". Without such functionality, our life would be a nightmare.
A cognitive habit is an habitual way of thinking about the same situation without really thinking. Examples: I need to do a phone call I will ask my partner to do it, They want me to speak I will say no, When I call someone I will stutter, I will never be more fluent, Without my stuttering I would have achieved more. All these habitual thoughts are done without any pressure from a situation, i.e. there are no 50 people looking at you or the person on the phone is waiting or you are feeling a block coming. No, you are under no pressure, but you have pre-prepared lines of thoughts for certain situations.
Cognitive habits are easier to tackle by re-thinking one's constructs. Automatic habits are much more difficult to change.
"Professor Johnson is shocked by the vicious smear campaign againt him from
former colleagues who now suddenly question his professionality. Throughout his
professional life as a hard working and well-respected university professor,
Professor Johnson has sought to advance our scientific understanding of
stuttering, and provide people, and especially children, who stutter with the
best care possible. His insightful research project has been a turning point in
improving treatment for stuttering and widely applied even 50 years later.
Moreover, it is important to note that this project has only come after years of
fruitless search for a neurophysiological cause for stuttering. Unlike many of
his colleagues, Professor Johnson had the courage to realise that the hopes for
a neurophysiological cause were unfortunately unfounded, and had the courage to
develop a new theory, namely that stuttering is of psychological origin, which
is supported by facts. Therefore, together with other experts including
statisticians they developed a carefully designed and monitored experiment to
test the theory. When Yairi and Ambrose attacked Professor Johnson's project in
The Journal of Fluency disorders, they not only had to base their arguments on
second-hand information, but were inconsistent in their criticism. They claim
great danger for the children, but at the same time claim that no children were
harmed and none became adult stutterers! This in fact shows how carefully
Professor Johnson's team has been! In fact, probably due to a lack of proper
research of the topic, they have missed a crucial element, namely that Professor
Johnson has made sure that the children immediately received special care after
the end of the trial. Moreover, he has even stayed in contact with some of them,
being a mentor and friend for years to come. As a parent of two kids himself,
Professor Johnson has always sought the best possible for his patients and
points out that his scientific work has been able to bring improvements in the
life of people who stutter. He finds it unfortunate that certain quarters of
academia and therapists are still clinching to a neuro-physiological cause,
which is unfounded by facts!" (Disclaimer: This text is a work of fiction, and does not represent anyone's view not even the author's!!)
Go ahead what would you say to Johnson's lawyer's statement?
Friday, January 20, 2006
In 1939, a controversial study on the possibility of "creating a stutterer" was conducted by University of Iowa speech pathologist Wendell Johnson and his graduate student Mary Tudor. The study tried to create stutterers over the course of 4 months, using 22 unwitting orphans from the Soldiers and Sailors Orphans’ Home in Davenport, Iowa. Ethically acceptable at the time, it was designed to induce stuttering in normally fluent children and to test out Johnson's "diagnosogenic theory"—a theory suggesting that negative reactions to normal speech disfluencies cause stuttering in children. The study divided the orphans into 3 groups: 6 normally fluent orphans would be given negative evaluations and criticisms regarding their speech, another group of 5 orphans who allegedly already stuttered would also receive that treatment, and the remaining 11 would be treated neutrally. The study concluded that the children given negative evaluative labeling went on to develop persistent, permanent stutters. The study was influential at the time, with many speech pathologists and child-health and educational professionals accepting Johnson's theory. In 1988, Silverman first reported the results of this study in the Journal of Fluency Disorders and labeled it "The Monster Study." While the information was well known to professionals in the area of stuttering, it was not until 2001 when the information was distributed to the public in a newspaper article. In June 2001, the San Jose Mercury News revealed this study to the public for the first time, leading to widespread controversy and debate about scientific ethics. Soon after, University of Illinois professors Nicoline Ambrose and Ehud Yairi wrote a paper discrediting the 1939 study, revealing flaws in data collection and method, as well as pointing out that none of the orphans actually did develop a permanent stutter. While criticism of a developing child's speech can certainly make a present stutter worse, it does not create a stutter.My comments in my next post!
His poem "complains" that during our discussion we treated people as a number and not as people! So I wrote him a poem back! Here it is. Dont be too critical with me. It is my first poem! Sorry it is in German...
Der Klippel auch wenn er's nicht gerne mag
lebt auch als Sammlung von Atomen Tag fuer Tag
Er verspuert sich wohl als stotternde Einheit,
Ist berueht von deren Geistes und Seelesfeinheit.
Doch, bitte schoen, soll er nicht vergessen,
Wer der Krankheiten weiss sich zu messen.
Es ist die Wissenschaft, die stets rational
Sich erweist des Unerklaerten Todespfahl.
Drum soll er uns streiten lassen,
Und vor unserer Aufopferungsgabe erblassen!
Le poete Tom
Thursday, January 19, 2006
The author asks "Why did the window break?", and offered the following answers
A) "Because the brick hit the window.",
B) "Because Tom threw the brick.",
C) "Because the window glass was brittle."
He also gave the following definition: The English ‘cause’ suggests efficient causation, some factor present in a situation that actually brings about a change
This makes me think that causes can be classified
1) Into EVENTS or STATES. Event: Brick hit the window or Tom threw the brick. States: Glass was brittle.
2) Into HOW CLOSE TO "breaking the window". For example, The brick hitting the glass is a more direct cause than Tom throwing the brick.
3) Into WHETHER THEY ARE SUFFICIENT to "breaking the window". Some causes are a necessary but not sufficient conditions for the change "window breaks". For example, the glass needs to be brittle for it to break, but you need some extra i.e. the brick hitting the glass.
So "Why do people stutter?"
Wednesday, January 18, 2006
As a kid I was good at sports. But, I was terrible when it came to swimming. I couldnt swim well, not because I was unfit, but because I was not able to apply the breathing techniques well to do crawl. Why? I somehow developed this habit of choking when I tried to breathe into the water. So after a few strokes, I couldnt continue and gasped for air. Four years ago, I started swimming regularly. It took me nearly four years to get rid of this choking habit. Now I can swim crawl without problems. Parodoxically, even when I try to choke, I cant anymore... The unlearning of this habit came very slow.. Stage One, I tried to change and the choking was worse. I hated swimming crawl. Stage Two, I was able to swim longer without choking, but still experiencing a feeling of being uncomfortable and of having to choke any second. Stage Three, once a while I started choking again, and I was pissed off and switch to breast stroke. Stage Four, I was able to swim without choking, but still felt a bit nervous. Stage Five, I just swam without thinking about it. Stage Six, I realised that I conquered it and saying to myself "I got you. Come on. I challenge you. Make me choke!" I can now confirm that I am a recovered choker, but I am not sure whether I am cured! :-)
I hate to think that unlearning stuttering habits is probably even harder...
Tuesday, January 17, 2006
So how about in the field of PDS? Here is Tom's ...
Are you a crackpot? test
1) Do you have a cure for stuttering?
2) Have you cured yourself from stuttering?
3) Did you have an inspirational moment, where suddenly you instinctively you knew what stuttering is really about?
4) Do you often refer to big names to agree or disagree with them like "I agree with Freud that..." or "I disagree with van Ripper that..."
5) Do you dismiss brain imaging and genetics studies as irrelevant without having read the research articles?
6) Do you think that people ignore your ideas to protect their own interests? Or that there is a secret conspiracy against you and your ideas?
7) Do you firmly believe that PDS is purely psychological?
8) Do you write a blog making comments about PDS research even though you only have a PhD in theoretical physics? (quote from a university professor)
9) Do you talk, talk, talk, talk, talk, talk, talk, talk, talk about your experience instead of asking others about theirs?
10) Do you over-use words like holistic, in-touch-with-oneself, and so on?
If you have answered more than three questions with YES: Congratulations!, you are a crackpot! :-) Please note that a university degree or a professorship does not neutralise the results, as experience shows in physics.
Here are the solutions:
1) There is no cure that works for everyone.
2) You might well have become fluent through hard work or / and an X event, but you are not cured in the sense that you have the same speech system as normal people.
3) You might well have had such a moment, and as a consequence became more fluent, but that does not mean that you understand PDS. You can very well become fluent by using a wrong theory of PDS. Like someone who thinks the treatment is a cure will be more successful that Tom who knows about relapse and so on.
4) Science is about strength of arguments and not about who made an argument. Personally, I couldnt care less about who said what. For example, in my field of physics, I have never heard any of the world leading people say "Einstein said that...". All the so-called authorities in PDS are just human beings who also make mistakes. And then again, why does someone become an authority??
5) Dismissing this kind of research without trying to understand it is just insane.
6) They might well protect their interest, but that doesnt make your theory right! Because if your theory is wrong, they would have behaved in the same way!
7) There is now so much research on brain and genes that this position has become untenable.
9) If you start talking to other people, you will realise that your stuttering is very different to others, and that generalising your situation or building a theory only on your experience is not possible.
10) These terms are very vague and not useful for a scientific discussion.
Sunday, January 15, 2006
Silverman, E. M. (1975). Speech fluency fluctuations during the menstrual cycle. Journal of Speech and Hearing Research, 18, 202-206.
Abstract: This study sought to determine whether changes in disfluency characteristics accompany biological and emotional changes during the menstrual cycle. Four extemporaneous speech samples were collected from each of 12 women, one at ovulation (when the average woman experiences her greatest feelings of self-esteem and self-confidence) and one at premenstruation (when she experiences a significant increase in anxiety level) for two consecutive cycles. The mean total frequency of the women's speech disfluencies produced at premenstruation was significantly greater than the mean total of their speech disfluencies produced at ovulation. The disfluency type that accounted for much of the difference in total frequency of disfluency between the two cycle points was revision-incomplete phrase. The tendency for these nonstutterers to produce more speech disfluencies at premenstruation than at ovulation is similar to a tendency we have observed in stutterers
Silverman, E. M., Zimmer, C. H., & Silverman, F. H. (1974). Variability of stutterers' speech disfluency: the menstrual cycle. Perceptual and Motor Skills, 38, 1037-1038.
Abstract: Studied whether women who stutter produce more speech disfluencies at premenstruation (when anxiety level has been reported highest) than at ovulation (when anxiety level has been reported lowest). 4 speech samples were collected from each of 4 Ss, one at ovulation and one at premenstruation for 2 consecutive cycles. Results show that Ss produced more disfluencies premenstrually.
Thursday, January 12, 2006
Here is Tom's oracle for major research events in 2006 and what they will find:
1. Brain imaging studies of teenagers, children who stutter, and adults who have stuttered as children: They will probably show that structural abnormalities already exist from very early onwards, and that children and adults who recover also have structural abnormalities.
2. More detailed genetics studies: Past studies have localised the responsible chromosomes for specific cases. They will localise the genes on these chromosomes. The function of the gene(s) will probably be building a protein that is (partially) needed to direct the development of language and speech areas in the brain.
3. The pagoclone study: The results will be very mixed. Some experiencing great improvement, but other none at all. Side effects will exist but relatively small. Leaving everyone do wonder why the hell it works for some and not for others? The company will probably go on with the next phase of trials, but instead of a cure they will focus their message on "Pagoclone works for some very well and for others not at all. You need to try it out with your doctor to see whether it works for you."
Within the next five years, 2010:
1. Medication (possibly Pagoclone or others) will become available. It will prove not be a perfect cure, but alliviate severity for most and considerably for some. There will be more clues as to why medication works for some more than for others. Possibly subtypes are identified by other means, or effect of medication will be used to define subtypes.
2. Brain and genetics research is now 15 years old, and the field will have come to a consensus on the broad features of PDS within the brain and the genes.
3. Meta-analysis is finally becoming more important in fitting everything together, because by now experimental evidence is detailed and plenty enough to be able to construct good theories.
4. Most early baby-boomer professors / therapists with old (anti-brain and so on) ideas will finally be in retirement leaving the way open for new people. (I do not mean all professors, just some! :-)
5. Other brain disorders will have been sorted out giving clear directions on within which framework to think about PDS.
Wednesday, January 11, 2006
Let me first say what I believe is the maximum understanding and treatment we can achieve: (I will talk about timeline in my next post)
1) PDS is very likely not a local problem but a more distributed problem. I give an example: it is not like computer hardware breaking down due to a faulty cable or a software with a bug in the code, but it is more like a very inefficient transport system or a high crime rate in a city. You will never be able to answer the question: Where exactly is the problem? You see the effects, but many factors play a role like the underground trains are very old, only one underground line, and the unions block any change. Currently, we don't even know what the various factors are. It's like, the city is still very foggy, and we slowly need to get rid of the fog (also due to genetics and brain imaging tools) and explore the different factors. The maximum understanding will come when there is no fog anymore, and all factors and how they interact are known.
2) There will not be a cure in the sense as having the same speech system as normal speakers, but more like the children who have recovered. Much greater fluency will be achieved faster with fewer relapse. Thus, it will not be like the computer doesn't work due to a cable failure so lets replace the cable or the computer bug is here lets replace this line of code. It is more like lets improve the inefficient transport system. God knows where you should start. So build a new underground line or lets get new trains. BUT the problem is that you cannot shut down a city (or a human being) for a few months and re-build everything. You can only do slow step-wise improvements. In therapies you always need to work on a change in behaviour, but with no fog around the city anymore, we will know much better where to attack the problem (which might be slightly different for different people). Medication is probably the most straightforward way to help people, as you just take a pill and nothing else. You don't need to follow some therapy which is much harder. Taking a pill will change neurotransmitter level in the brain and is like ensuring that there is never bad weather in the city or the people using the transport system are not stressed. And the transport system improves tremendously (without solving underlying issues), but is not really a cure as such.
Actually, to be completely honest with you, I think that in 9999 there will be no human beings anymore as we know now. So there will also be no stuttering anymore!! We will have morphed with computers into one big system. We will be sub-entities like cells in our body. And communication between sub-entities (direct descendants of us) will not involve speech anymore. This process has just started with the Internet. For example, take my blog, I am currently putting ideas into your mind, and you can influence my mind by posting comments. These comments are just like my own thoughts: I might take them on or ignore them. Wikipedia and google have also dramatically increased our common shared memory and so on. This process will continue... :-)
Monday, January 09, 2006
Here is another interesting talk on preliminary brain imaging results by Kell, Neumann, and Giraud: I know Katrin Neumann and I have spoken to Anne-Lise Giraud once. I googled Christian Kell, and he is most web-famous for scanning the cortex representation on the penis! See here. Apparently, the region is very small! (contrary to the commonly presented picture! See above) Dispelling the terribly dangerous myth created by sexist females that men are controlled by their... I am wondering whether Kell finds his research of PDS as exciting?! :-)
The researchers from Frankfurt claim that prosodic production tasks during fMRI reveal functional deficits in stutterers. Prosody can be defined as the patterns of stress, intonation and timing in a language. They say that both groups with or without PDS show similar performances, but have different brain activation. I am not sure what to think. From my personal experience, I seem to be far more fluent when I actively control the prosody of my speech. It feels a bit like singing, or chorus reading. So even if abnormal, the prosody neural network seems to help me to be more fluent. But of course, this might only be the case when I actively control my prosody and on automatic mode it becomes unstable? How does this fit with the dual premotor systems hypothesis Per Alm has been advocating: see here? Not sure how their results would fit in. I don't think they have published the findings yet. I guess they are in the review process.
Here is the abstract:
Persistent developmental stuttering can be interpreted as the result of impaired linguistic motor executive function. Previous studies revealed pathologies in somatomotor as well as language-related cortices of stutterers. Frontal opercular regions (Broca and its right-hemispheric homologue) appear differentially activated in stutterers when compared with healthy controls. Stutterers seem to compensate their defect spontaneously via an activation of the right frontal operculum, while after fluency-shaping therapy a more left-lateralized frontal activation can be observed. Based on these findings, we sought to preferentially activate either the left or the right frontal lobe. Prosody perception usually involves lateralized cortical networks depending on whether it emphasises linguistic or emotional features. We therefore hypothesized that a similar functional lateralization should be observed in frontal regions during speech production emphasizing different prosodic features. While production of linguistic prosody should predominantly activate left-hemispheric regions, emotional prosody should reveal a more right-hemispheric network. The production of linguistic prosody should therefore reveal in a very selective manner relative left-hemispheric deactivations in stutterers, while production of emotional prosody should tell us more about the functional meaning of right frontal overactivations in stutterers relative to controls. After confirming functional lateralization of spoken prosody in normal subjects we compared activations in stutterers and controls. Despite similar behavioural performances, we found a very circumscribed left frontal deactivation in stutterers in the linguistic prosodic task in BrocaÂs area. The emotional prosodic task activated larger fronto-temporal networks in stutterers, but no significant differences were found in the group analysis. Our results delineate a focal functional lesion in the stutterersÂ left language executive network, which may require compensation by BrocaÂs right homologue.
Sunday, January 08, 2006
Mark Jones et al. have responded to the rapid responses, but they have not directly responded to the arguments put forward in my rapid response. For example, they say that
"... spontaneous recovery has been a recurring theme in the rapid responses to our article... The rate of natural recovery from stuttering in young children in the general population has been estimated at 74%(1), but in clinical populations with this condition this estimate is expected to be much lower...Evidence from a previous study(2) suggests that approximately 40% of children identified as stuttering had the condition for less than 6 months."However, they do not directly relate this or other statements to my arguments to disprove my case, so it is difficult for me to respond in a constructive way. My guess is that they imply that any effect due to the spontaneous recovery rate on the statistics is very small because the rate in the clinical setting is only about 40% and not about 75%. But this argument is not correct. The great irony is that the closer the recovery rate is to 50%, the greater the impact on the statistics!! :-) So by claiming a 40% rate instead of a 74%, they have actually strengthened my argument that they need to revise the statistical significance and effect size of their study to take into account the natural recovery rate!
I have sent a response, where I explain in more details. The response should be on-line in one or two days. Check here.
Saturday, January 07, 2006
Here are my New Year Resolutions:
1. Keep on writing posts at the same pace. Might be tough if I get more busy job-wise.
2. Try to get a few promiment researcher write a few posts.
3. Re-design the blog layout and functionality a bit. I might include a stuttering brain in the header. If you have any suggestions, feel free, especially if you are the creator the French website Paroles de bègues! :-) I am also thinking of generating a bit of money to cover my costs and time spent. I am not sure about a google AdSense button. But I might add a Donate button in case a millionaire wants to donate some money! :-)
4. I am also thinking about launching a website to include a discussion forum on research, archive, lists of researchers, and more. I have already a precise idea and a project plan. But just need the time and focus to do it. Maybe it would be good to get more people involved in such a project. But teams (and committees) are typically nightmares and compromises virtually always worse outcomes that either of the two competing proposals!
5. To be a bit more serious on reading the PDS literature.
I did an interesting test. I took the data from all the patients of the Kassel Stuttering Therapy database, and plotted their fluency data with respect to the month they were recorded to see whether there is a seasonal difference. For example, may be we stutter more during the winter then the summer? But I did not find any strong signal, but this might due to methological problems. The data is not well normalised, i.e. some months might have more severe stutterers.
Friday, January 06, 2006
BUT Per Alm's following comment has triggered a paradigm shift in my thinking:
What is important to point out is that observations of other possible impairments, for example of language ability, very well may be an "epiphenomenon", that is, a phenomena that occurs in parallel with stuttering but that is not causally related to stuttering. All too often reports of differences between stuttering and non-stuttering persons are interpreted as causal, when they are more likely to be just epiphenomena.
In the back of my mind, I always thought of the lower performance of people with PDS in dual tasks like finger tapping (research by Webster, de Nil and Bosshardt), and language skills (research by Christine Weber-Fox) as collateral damage to PDS. I never gave it too much importance. But now suddenly I find this research and the related insights very exciting, very important and crucial for the bigger picture of PDS! Why?
My current thinking (and of the few people with the same wavelength) often is based on two views:
1) We concentrate on stuttering either as the symptom of overt stuttering or concentrate on the brain mechanism that leads to stuttering.
2) We view stuttering as the disorder, and PDS causes or also includes much more subtle deficiencies like dual tasks, language deficits, etc.
But now I think that is a very biased way of looking at the issues. And the two views should be:
1) Overt stuttering is a (but not necessarily the only) consequence of PDS and PDS is a (but not necessarily the only) consequence of X.
2) X causes many different functional deficiencies like PDS, language deficits, dual task deficits, and possibly more. PDS is only the most visible due to its importance in human activities, and a compensating mechanism only works well in 80% of the cases but only partially compensates in the remaining 20%. Then the 20% face enormous pyschological and social pressure, because they do not function normally, "normally as defined by the environment they live in" and their reaction to their stuttering is very strong leading to even more severe stuttering, bad habits, and so on. Were subtle dual tasks as crucial for human activities like speech, we would be dys-dual-tasking.
X is a structural deficiency/abnormality happening during the development of a brain region(s) caused either internally by genes or externally by some neurological incidents (or even due to some rare extreme traumatic experience).
X exists in all developmental brain disorders. X can happen in all kinds of brain regions due to all kinds of genes leading to different disorders. X may cause or increase likelihood of development of PDS, dyslexia, and dyscalculia (spelling?), for example. Everyone has some X somewhere, but often the structural deficiencies lead to non-detected subtle functional deficiencies, because they are not important for our functioning (in our society). For example, 10'000 years ago no-one would have cared about dyslexia, and there would have been no opportunity to see it in a society without writing and reading! So X is not really a disorder as such but just nature experimenting with different gene setups. And the society and the environment will select out genes that cause the Xs which lead to significant handicap impairing chances of re-productivity.
OK. I better stop here. I will read this post again tomorrow to see whether this is all nonsense or a beautiful new paradigm of looking at PDS. :-)
As far as I know, there are three groups that are actively recruiting and scanning kids. The group around Katrin Neumann at Frankfurt, Kate Watkins at Oxford, and Soo-Eun Chang at NIH. All three groups are linked to "scanning factories" with considerable experience and expertise. So the research should be of a high scientific standard.
Sofar, just Soo-Eun Change et al. have communicated preliminary findings, as I have discussed here and here.
Once all three have published papers, which as always might take years with the secretive, out-dated, time wasting and often pretty useless current peer review process (that could not even deter the significant fraud of Prof Hwang on stem cells), the fog will clear further, and we will have a much better understanding on how PDS works.
Wednesday, January 04, 2006
There are two reasons for better progress in neighbouring areas. Much more money is going into these areas (dyslexia, schizophrenia or Tourette syndrome), and research is generally more scientific than in PDS and not as laden with foggy swampland of psycho-stuff for several reasons. I also think that it is a scandal that so much money has gone into other brain disorders and so little into PDS. We need to shout louder when it comes to getting a share of the research money!!! Remember when you shout, you don't stutter!!! So start shouting! :-)
Here is the description of Science:
Miswiring the Brain
Although dozens of genes have been linked to brain disorders in recent years, connecting the dots between genetics and abnormal behavior has been anything but child's play. This year, however, researchers gained clues about the mechanisms of diverse disorders including schizophrenia, Tourette syndrome, and dyslexia. A common theme seems to be emerging: Many of the genes involved appear to play a role in brain development.
In November, two reports put meat on the bones of previous claims that variants of a gene called DISC1 increase the risk of schizophrenia. One research team found that inhibiting DISC1 activity in mice alters brain development, causing subtle abnormalities in the animals' cerebral cortices similar to those seen in postmortem brains from schizophrenia patients. Another team linked DISC1 to molecular signaling pathways important in brain development and in regulating neurotransmitter levels, which are often out of whack in psychiatric patients.
In October, researchers described a rare genetic defect that appears to cause Tourette syndrome. The mutation likely causes only a tiny fraction of Tourette cases, but its discovery may be an important lead. One gene that's disrupted, SLITRK1, influences branch formation by neurons and is active during development in brain regions thought to be altered in Tourette syndrome and other conditions, including obsessive compulsive disorder. New research also links developmental genes to dyslexia, identifying three genes--KIAA0319, DCDC2, and ROBO1--that may cause faulty wiring in neural circuits involved in reading.
Much of the new work suggests that genetic miscues, rather than causing neuropsychiatric disorders outright, alter brain biology in the womb in a way that predisposes us to problems later in life. A better understanding of how this happens may help reduce the risks. (Science website)
Tuesday, January 03, 2006
Monday, January 02, 2006
Here is the abstract:
Cerebral lateralization of speech processing in stutterers were assessed with noninvasive brain imaging techniques, magnetoencephalography and multichannel near infrared spectroscopy (NIRS), with which neuromagnetic and hemodynamic responses, respectively, were recorded to analysis-synthesized prosodic and phonemic minimal contrast word trains. Adult stutterers did not show normal leftward dominance for the phonemic contrast with either method. Children underwent only NIRS sessions, with results similar to those of adults, which indicates that the cerebral dominance in processing heard speech is in disarray even in school-age stutterers. NIRS method may be useful in screening young stutterers and in elucidating neural correlates of stuttering.
Strangely enough or as expected, their research has neither been replicated nor commented on by the "Western establishment". To me, their findings are at least interesting enough to be criticized! :-(
... These previous [brain] studies, however, have been limited to examining only adults who stutter, and no studies have thus far examined neural correlates of spontaneous recovery from stuttering. Hence it remains a clinically and theoretically imperative goal to determine the neural correlates of childhood stuttering persistence and recovery, closer to disorder onset.
Here we present preliminary results from a voxel-based morphometry study
(VBM) looking at children with persistent stuttering (CWPS), children who have spontaneously recovered from stuttering (CWRS), and children who have never stuttered (CWNS). Results indicate that, compared to CWNS, children who persist or have recovered from stuttering have significantly less gray matter density in the left hemisphere inferior frontal regions coinciding with the Broca¹s area, as well as the anterior cingulate. Interestingly, CWRS showed an intermediate level of gray matter density compared to CWNS and CWPS in these areas. Results are discussed in context of possible developmental pattern differences that lead to, or are a result of, eventual persistence or recovery from stuttering.
The present results point to anomalous gray matter density (GMD) in several regions of the brain as possible neural correlates of developmental stuttering. Regardless of eventual persistence or recovery, children who have once stuttered appear to exhibit significantly reduced GMD compared to their normally fluent peers in areas such as the left IFG, an area known to be critical in speech motor planning. Although CWRS generally showed a similar pattern of GMD findings to CWPS, they also exhibited important differences from the latter, which may reflect brain plasticity associated with natural recovery from stuttering. For instance, CWRS tended to exhibit an intermediate level of GMD in the left IFG and ACC, namely, levels of density approximating that of controls. On the other hand, CWRS tended to have decreased GMD in parietal regions such as the SMA (BA 6) and the SMG (BA 40) compared to the other two groups, possibly reflecting the effects of increased pruning in these regions correlating with a compensating mechanism they may have adopted to aid in recovery.
This study has several limitations. First, due to the small sample size in the three groups (n=7 in each group), the results are preliminary and need to be replicated with a larger sample. Second, although VBM provides an even-handed approach to looking at regional differences among groups on a whole brain basis, the process of averaging and smoothing involved in the analysis pipeline may obscure individual differences in structure, and group differences in smaller areas of interest may be more difficult to identify. Third, structural anomalies may merely represent risk factors for anomolous function. As such, future studies may consider pairing structural techniques such as VBM and DTI with functional techniques (i.e., fMRI and MEG) in order to elucidate correlations between anomalous structure and functional deficits involved in development, maintenance, or recovery from stuttering.