Monday, August 22, 2016

Watch Area 44 and not Area 51!

Looks like a very interesting piece of brain imaging work by the Martin Sommer team with the main author Nicole Neef here:
Area 44 is a cytoarchitectonically distinct portion of Broca's region. Parallel and overlapping large-scale networks couple with this region thereby orchestrating heterogeneous language, cognitive and motor functions. In the context of stuttering, area 44 frequently comes into focus because structural and physiological irregularities affect developmental trajectories, stuttering severity, persistency, and etiology. A remarkable phenomenon accompanying stuttering is the preserved ability to sing. Speaking and singing are connatural behaviours recruiting largely overlapping brain networks including left and right area 44. Analysing which potential subregions of area 44 are malfunctioning in adults who stutter, and what effectively suppresses stuttering during singing, may provide a better understanding of the coordination and reorganization of large-scale brain networks dedicated to speaking and singing in general. We used fMRI to investigate functionally distinct subregions of area 44 during imagery of speaking and imaginary of humming a melody in 15 dextral males who stutter and 17 matched control participants. Our results are fourfold. First, stuttering was specifically linked to a reduced activation of left posterior-dorsal area 44, a subregion that is involved in speech production, including phonological word processing, pitch processing, working memory processes, sequencing, motor planning, pseudoword learning, and action inhibition. Second, left posterior-area-44-to-parietal functional coupling was deficient in stuttering. Third, despite the preserved ability to sing, males who stutter showed bilaterally a reduced activation of area 44 when imagine humming a melody, suggesting that this fluency-enhancing condition seems to bypass posterior-dorsal area 44 to achieve fluency. Fourth, time courses of the posterior subregions in area 44 showed delayed peak activations in the right hemisphere in both groups, possibly signaling the offset response. Because these offset response-related activations in the right hemisphere were comparably large in males who stutter, our data suggest a hyperactive mechanism to stop speech motor responses and thus possibly reflect a pathomechanism, which, until now, has been neglected. Overall, the current results confirmed a recently described co-activation based parcellation supporting the idea of functionally distinct subregions of left area 44.
Area 44 seems to be a kind of orchestra conductor, which goes somewhat into recent suggestions (and my belief) that stuttering is a system failure, i.e. that it's not necessarily a single function (in one area) breaking down but the system of different interacting areas as a whole but in this case it's one area that is needed to orchestrate the system. But I have to say that I do not know enough about this topic to make more informed comments.

Tuesday, May 31, 2016

RESTART DCM workshop in Rotterdam in July 14-16th

Marie-Christen Franken has written to me regarding a workshop she is organizing in Rotterdam:
This July we will have an International RESTART DCM workshop in Rotterdam, so far 14 clinicians from all over the world have subscribed for that. We could book about 6 or so more. Maybe you would like to bring this to the attention of colleagues who might be interested?
You can view the invitation here.

Tuesday, May 17, 2016

Walking, talking, and sharing in the French Pyrenees with Paul

If you enjoy walking in wild natural environments, eating good food, and sharing your experiences with other like-minded people, this is for you!

In 2016 Paul Brocklehurst and Blanca Rubí are hosting a week-long retreat in the Pyrenean mountains, close to the French-Spanish border. Our aim is to provide opportunities for small groups of up to 10 people, all of whom have a connection with stuttering, to walk, talk, and share experiences in the midst of one of the most spectacular and beautiful natural environments that Europe has to offer.

There are still spaces free on the walk and talk. Both PWS and their partners welcome.

Sunday, May 15, 2016

No, a quick cure for all is far away.

The author of this article is completely misinterpreting the likelihood of a cure: read here.

But of course that will prevent virtually no mainstream journalist and desperate pws to jump on the bandwagon.

Let me clarify the stuttering mouse hype:

1) this mutation as far as I understand occurs in 5% of all people who stutter. So even if those people could be cured, the remaining 95% would not.

2) even if the mutation is proven to cause it and we would know the causal link between mutation and neurobiology vulnerable to jams in the brain, there is no guarantee that the damage done by the mutation change be counteracted.

3) even if an antidote to the mutation can be found, e.g. by providing the body with the missing proteins that the mutation did not produce, the protein might have been critical for proper development of neurobiology and thus will only help children who are developing their neurobiology but not adult brains. A bit like it is too late to use better cement once the house is built!

4) even if an antidote exists, it is not clear whether it has side effects.


1) a hype for a cure, even if completely misguided, could lead to political pressure to put much more money into stuttering. Why are you financing stuttering research, you terrible politicians??? Do you want to be responsible that little stuttering kids are cured?

2) it is the first example of proving that genes are correlated with stuttering behaviour and untangling the causal link will definitely help us understand at least 5% of stuttering.

Tuesday, April 19, 2016

"Stuttering" mice make us fluent?

They managed to create a stuttering mouse, or let be more precise they created a mouse that has the same gene mutation than a subclass of people who stutter and that shows an abnormal "speech" pattern.

This is significant as we are moving out of the soft psychosocial research arena with weak research standards to a more rigorous research arena with full-time scientists who have been trained to this kind of stuff for many different disorders.

I predicted this development at the discovery of the gene mutation.

Read the article in Cell here.

Thursday, February 18, 2016

BREAKING NEWS: The era of sub-typing has started!!!

OK, I am a bit late at responding but there are exciting new developments in the genetics and brain imaging of stuttering. And you should listen to StutterTalk's Peter Reitzes interview with Denis Drayna, but listen carefully and rewind a few times as he throws around all kind of protein names.

The essence is: We have found another protein complex (affected by other gene mutations) that disturbs the normal functioning of a nerve cell in very similar aspects as the previously found protein complex. Imagine you find that the postman has a limp and then you find that the postman's car is slow so you can argue that it is about the slowness of the mail delivery that is at the core of the problems. And that is also what Dennis suggested: at least some stuttering might be part of issues with "moving things around in the nerve cells (which can be quite long)" which are suspected causing all kinds of neurological disorders.

And I am happy to hear that they do what I asked them to do: Only brainscan people with the same mututation! This is the way forward in my view.

Of course we need to be careful:
  • not all stuttering is driving by this.
  • neurodevelopmental issues could affect similar areas but are driven not by gene mutation 
  • Dennis knows much more about but again we have to wait years until he publishes it. ;-)

Will I meet you in Antwerp on February 27th?

Wednesday, February 03, 2016

What Causes Stuttering with Dr. Soo-Eun Chang

Check out Peter's interview with Soo-Eun Chang, who is a neuroscientist from the Speech Neurophysiology Lab at the University of Michigan and specializes in brain imaging young children: here.

If I get time, I will listen to the interview in full and make comments. After only 5 minutes of listening, I already have a different take on some statements! ;-)

Sunday, September 13, 2015

How does Lidcombe work? No as they thought it would!

Lidcombe is apparently the miracle treatment for young stuttering children. A recent study by Franken et al. showed that another treatment based on Demands & Capacity theory is equally effective than Lidcombe, a behavioural therapy.

Many times I have said that I am not convinced that Lidcombe treatment is more effective than natural recovery, but they do claim that for a short-term control group the treatment group does much better. And I currently argue: yes that is true but only for those that would have recovered any way AND the therapists and kids know that they are being treated AND the kids know what is expected of them.

Of course, if Lidcombe claims to be a miracle treatment, I expect that they tell me what causes the miracle. And here, I say: they will not find anything. Many outcome studies of psychotherapies have shown that anything can work and that the key success factor is the patient-therapist interaction.

I often criticize the Australian but they did the right trial to look into it. An article on An investigation of the role of parental request for self-correction of stuttering in the Lidcombe Program. by Donaghy, Harrison, O'Brian, Menzies, Onslow, Packman, and Jones gives the answer I expected: nothing.
METHOD: Thirty-four parent-child dyads were randomized to two treatment groups. The control group received standard Lidcombe Program and the experimental group received Lidcombe Program without instruction to parents to use the verbal contingency request for self-correction. Treatment responsiveness was measured as time to 50% stuttering severity reduction. 
RESULT: No differences were found between groups on primary outcome measures of the number of weeks and clinic visits to 50% reduction in stuttering severity. 
CONCLUSION: This clinical experiment challenges the assumption that the verbal contingency request for self-correction contributes to treatment efficacy. Results suggest the need for further research to explore this issue.
So what really drives the treatment outcome?

And the same question goes to the Demands & Capacity treatment.

Friday, September 11, 2015

Amino acid supplementation seems to have worked for one reader

I get many emails from readers telling me about significant changes in fluency. One of them is John and he agreed to share his story with us. Read below about his search for an explanation to his sudden fluency. He would be happy to discuss via email: 

Like a lot of people who stutter, as I am told, I frequently experience issues with low mood. On about my 15th effort to find a solution for this, I started supplementing with various amino acids to target various neurotransmitters, specifically the ones known to cause mood issues (e.g. serotonin, beta endorphins, dopamine, etc.). Quite unexpectedly, after using these supplements, I noticed a marked drop in stuttering, on the order of about 90% most days (some days 100%). I found myself being able to have conversations with people where I was talking a solid 20-30 minutes without a single stutter. Even the people around me remark that "it" is just "gone". I have stuttered for over 30 years, and this had never happened, especially for this long (I have sustained these effects for about 15 months now). I have tried on my own, as a hacky citizen-scientist, to try and piece together what I have observed. What I *think* is happening is some sort of synergistic process between boosting both dopamine and beta-endorphin. Ironically, this sort of flies in the face with what I understand about he current pharmaceutical approaches to stuttering treatment, that is, trying to cut down on available dopamine. What is amazing about amino acid supplementation is that, at least for me, there are zero side-effects. My mood is a ton better and my speech is a ton better. Of course, it could just be that, that my speech is better because I feel better, but I do see a definite increase in stuttering when I stop taking the aminos, even before I notice a drop in mood. What I would love to be able to do is be able to study this further. I would love to be able to work to understand what I have found, if I am just an anomaly, or if this sort of therapy holds promise for others as well.