Tuesday, June 28, 2005

I am off to Oxford

I am now leaving to Oxford. I wrote a long post in my text editor, but then my computer restarted itself out of the blue. I didnt have the automatic save on... So sorry there will be no post today... :-(

I might post from the Oxford Dysfluency Conference itself... Live coverage so to speak...

I will be back in a week's time and then there will be more serious posts!


Saturday, June 25, 2005

I cant remember how to stammer! Help!!

I am back from holiday. I went to Spain for a Swedish wedding and afterwards travelled through Andalusia. The Alhambra fortress / gardens / city / palace in Granada is very impressive in magnitude and style built at the times of Arabic control of Southern Spain: see pictures below. So are the bull fight arenas in Sevilla and Alicante, but I didnt see a fight.


He is asking whether the brain can forget to stammer in case of loss of memory. The answer depends on your theory of PDS and of which memory you are talking about. The word memory is too vague, as there are different types of memory located at different places in the brain. And there is working memory (up to 5 minutes), mid-term memory (up to two years), and long-term memory storage in our brains. There is explicit memory: factual (London is the capital of England), episodic (events in your life) and implicit: motor skills (knowing which muscles to move to skate or ride a bicycle), cognitive skills (chess, bridge).

What makes Tony's question so interesting is that putting on the "loss of memory" glasses would allow us to test (at least theoretically) different types of PDS theories if we were able to control memory loss temporarily. For example, if PDS is psychological and you temporarily erase of episodic memory of stuttering, the person should be completely fluent. If PDS is learned / bad habit, temporarily erasing memory of unnessary motor skills, would make the person fluent or at least eliminate unnecessary body motion. If PDS is purely a neurological weakness, memory loss will not affect stuttering.

My way of looking at PDS is as always: it's a neurological problem first, then acquisition of learned behaviour together with episodal memory of past stuttering. So yes, if you provoke memory loss, I think the person would improve his/her fluency but not be completely fluent and might develop memory producing more disfluency. For example, I think you can see this in kids who stutter or in older adults who have neurogenic stuttering i.e. provoked by stroke or similar illness. They do not have the memory of past stuttering.

I dont know how to knock out memory. I just know of the movie Eternal Sunshine of a Spotless Mind., where this doctor erases bad memories of your ex or your dog that died. Drugs acting on memory might be used for experiments but not for treatment, as the costs are far too great. I'd rather be disfluent that have no memory or be drunk all the time!!

In my next post, I will talk a bit more of Per Alm's PhD thesis that I read in more detail during my Spain trip.

Thursday, June 16, 2005

I am on holiday

I am off on holiday for a week.. So I wont be able to post.... I am going to take Per Alm's PhD thesis as holiday literature with me, so you can see that I am really obsessed by PDS... :-)


Monday, June 13, 2005

Social Anxiety

I am soooooooooo busy. I am going on holiday to Spain for a wedding on Thursday. Here is an interesting article that I have recently read: here . I think Prof Craig is a very good researcher. I always enjoy reading his articles.

He talks about Social Anxiety and Stuttering. He concludes with: "In conclusion, it is becoming clearer that a fluency disorder like stuttering, if it persists past the teenage years, is associated with higher levels of social anxiety. This is especially the case if their stuttering is severe enough to warrant therapy. It is also especially true for women. It is important that we should not be surprised that stuttering can cause distress serious enough to create social fears and anxieties. People who stutter should also be more willing to seek additional help that can offer professional guidance in helping them to control their anxiety. The future is in their hands."

I like his article as it quite surgically destroys the myth that people with PDS stutter because they are anxious to talk. NO! They stutter and that's why they become anxious and then sometimes stutter even more. At least that's my opinion. There is just one "criticism" or let's say comment. As a person who stutters, it seems obvious to me that people who stutter would develop social anxiety. If you cannot do something well but everyone else can and does not understand why, you will be concerned right? So why researching the obvious / common sense??? Am I being unfair now?

Wednesday, June 08, 2005

Are there phase transitions in PDS?

One way to look for solutions to a problem is to put on different glasses i.e. to analyse a problem using different concepts/viewpoints. For example, I have talked about the sex ratio and used this concept to analyse PDS. The last posts were about the basal ganglia putting it in the spotlight and understanding PDS around it. Today, I want to put on yet other glasses and analyse PDS from the point of view of phase transitions.

What are phase transitions? It is a concept used in physics to describe phenomena where a small change of a parameter leads to a dramatic change in the properties of a system. I give an example: water. If water is at 0 Celcius and you decrease the temperature by a very small amount, it freezes to ice immediately thus dramatically changing the properties of the substance. But if you cool water from 10 Celcius by a very small amount, it is still liquid just a big colder thus the properties change a bit and in a continuous way. Another phase transition is at 100 Celcius where liquid water goes into vapour (i.e. adding a bit more temperature (=energy), the water molecules have suddenly enough energy to overcome attraction to other water molecules).

My question is: Are there phase transitions in PDS?

You can look for phase transitions in many areas of PDS. The most obvious is to look at the difference between people with PDS and without. Can you unambiguously put someone into either the PDS or non-PDS box? OR, is there is a continuum, a smooth transition, from a severe stutterer to a fluent speaker. The transition in disfluency rate (as a symptom of PDS) between stuttering and fluent speakers seems to be a continuous one, and you can find the whole range of disfluent speech in all degrees of severity. Even "fluent" speakers are disfluent to some degree and stuttering speakers very fluent sometimes. There does not seem to be an obvious boundary when just looking at stuttered syllables. Most studies define stuttering as above 3% of stuttered syllables, but this is a rough guideline.

On the other hand, you immediately know when someone has PDS when witnessing certain symptoms like loosing eye contact, word substitution or grimaces, etc. I once asked Luc de Nil whether if I gave him a brain scan, he would be able to say whether the person has PDS or not. And he said yes. There is some research by Neumann & Preibisch that claims that the more fluent a PDS subject the more atypical right-brain activation, but fluent speakers show no right-brain activation. This would mean that there is a clear cut-off, and distinction between fluent controls and fluent PDS subjects. If there is a gene (as seems to be the case for some people), then it's discontinuous again, you either have the stuttering gene or you dont. Compare this to a dysfunction of the basal ganglia, Per was talking about the relative number of dopamine receptors. This is continuous again, as the ratio can be changed slowly, and a higher ratio just means less/more activity and more dysfluency. But, there could also be a cut-off point, where you have a phase transition i.e. a small increase in dopamine receptors is the last drop that lets the barrel overflow?

I could go on... I think it is an interesting concept to ask new questions about (the findings on) PDS.

Monday, June 06, 2005

More on basal ganglia

Per Alm has posted a long comment on my last post on whether the basal ganglia is involved in PDS. Click on "Comments" at the bottom of my previous post, or go directly using this link.

Let me summarise what (I think) he said.

1) The basal ganglia could well NOT be dysfunctional and still be involved in PDS as part of a wider system often called the basal ganglia-thalamocortical circuit, which would show dysfunction.

2) The fluency-inducing effects provide the strongest argument in favour.

3) Brain anomaly studies by Foundas et al, Sommer et al, and Jaencke et al. are interesting but too preliminary for final judgment.

4) But their findings could fit: "the basal ganglia generates go-signals based on the input from widespread cortical regions, but the input from the sensorimotor cortex can be assumed to be especially important. If the signals from the sensorimotor cortex to the basal ganglia are disrupted, distorted, or weak, the basal ganglia will not be able to do their part of the job. The result will be distorted output from the basal ganglia to the SMA, which will make it difficult for SMA to generate the final go-signals for the speech segments."

5) "Stuttering with adult onset has been reported after lesions in various parts of this circuit, like the basal ganglia, the thalamus, and the SMA. However, the characteristics of the disorder can be expected to be somewhat different depending on location and nature of the dysfunction. "

6) There is a lack of CLEAR experimental evidence as experiments have not been specifically set up to study basal ganglia effects and brain imaging studies have weaknesses.

7) But, "In fact, the meta-analysis by Brown, Ingham et al. did find differences in basal ganglia activation between stuttering persons and controls. The controls showed a weak left globus pallidus activation, which was not shown by the stuttering persons."

8) Per goes and gives an possible explanation for 7). [please refer to his comments for the details]

9) Factors within the basal ganglia might well increase or decrease the risk for stuttering in the proposed model like the number of dopamine receptors.

I still have to digest all his comments. Especially on brain anatomy, where I need to learn more about. I am also a bit reluctant to go into too detailed discussion as I don't want to loose every reader of my blog. But please feel free to post detailed comments.

But here are some challenges to Per, which might be hard to overcome:

1) Devise experiments that can unambiguously test aspects of the theory. For example, which experiments could be made that can FALSIFY the basal ganglia theory?

2) Show that the possible dysfunctions, that you state, of the basal ganglia circuit (which not only caters for aspects of speech that PDS affects) does not have any effects on other brain functions. This circuit seems to be rather distributed and entertaining many regions, and I find it hard to imagine a dysfunction not having more widespread effects. And I also find it hard to see why so many different factors result in basically the same symptoms.

3) Avoid arguments that are prone to logical fallacies. For example, I am a bit uncomfortable with Per referring to arguments like "different types of stuttering", "also other factors can influence", "the wider circuit", "several potential problems when studying stuttering by means of functional brain imaging". It might be true that many factors influence PDS or that there are different types, but then how can your theory be (or how can you make your theory) testable / falsifiable? It might be true that, as you state, there are several potential problems with brain imaging, but then how can you use brain imaging results to defend/falsify your theory?


Friday, June 03, 2005

It's (not) the basal ganglia, stupid!

Brown, Ingham, Ingham, Laird and Fox have commented on Alm's work: "[He] proposed a model in which the core dysfunction of stuttering was suggested to be an “impaired ability of the basal ganglia to produce timing cues for the initiation” of speech motor activity (p. 325). Unfortunately, this proposal provided no predictions about whether particular nuclei/circuits of the basal ganglia would be over- or underactivated during stuttering. [Our] meta-analysis data did not provide strong indications either favoring or opposing this model." They then go over various activitation signals in various experiments, and discuss its possible relevance to a dysfunction in the basal ganglia. But conclude that "Although the basal ganglia may certainly be playing a contributing role in stuttering, this role is in need of elucidation in future studies."

Doesn't look promising for PDS as they don't agree?? ON THE CONTRARY, I think this is GREAT progress in PDS research. At least to me! :-) Their (constructive) discussion shows that PDS research has moved closer to the core of PDS and research issues can FINALLY be decided by inconsistency or experimental findings, and not on authority or intuition. They are able to ask concrete and by-experiment answerable questions. They are able to do this, because brain imaging is delivering them DIFFERENCES between PDS and control subjects. So you can actually construct a theory and decide whether it is correct or incorrect. I find this very exciting.

So what's my view on the basal ganglia theory? Is it right or not? I have to admit, that I haven't YET read word-by-word Alm's theory and their article. So I might say something factually wrong. But, what I find very striking is that both works by Alm and Brown & InghamS et al. seems complementary. Brown & InghamS might have a theory (using partially efference copies) to understand brain activation patterns, but they remain silent of why and what it is that causes "failure to properly initiate the motor plan". And that's exactly the end product of Alm's work: "Stuttering is suggested to be caused by a disturbance of the medial system, in most cases in the basal ganglia. The core dysfunction is proposed to be impaired "go-signals" from the medial system, supposed to trigger the next motor segment in speech". BUT I am not sure he can explain why there should be brain anomalies as found by Sommer et al. , Foundas et al. , and Jancke et al. . And experimentally it seems to be on weak grounds, as Brown & InghamS say, "[Our] meta-analysis data did not provide strong indications either favoring or opposing this model." So it seems strong conceptually but no clear experimental signal, which should have been found by now??

So my pinch-of-salt is: The basal ganglia is involved but there is no dysfunction. To understand this, we need to talk about postmen! :-) Imagine two postmen are responsible for delivering your mail. But you only see one of them delivering mail to you. So you blame the other one for not delivering mail. But he might be a hardworking postman, but unfortunately he is the postman that your dog doesn't like! So both postmen are "functional", but it's your dog who makes the selection. The same might happen for the basal ganglia. It might work perfectly well and projects time signals into speech areas perfectly well, but that the area is not integrating them well. And this might be the anomaly area found. Paradoxically, most components of the basal ganglia theory would survive neatly like explaining fluency inducing effects i.e. the different system projects to a properly working area that integrates the signals well. Interestingly, factors that impact the functioning of the basal ganglia would still play a role, because a strong performance by the basal ganglia could well give PDS people enough timing signal to speak fluently, but a bad day or stress or emotions makes it worse. This would actually explain why the basal ganglia has not been singled out by experiments.

I am just making guesses, so please comment if you disagree. But I like this way of explaining things, and my brain has not YET found anything that rules it out.


Wednesday, June 01, 2005

Per Alm "blames" the basal ganglia

The good thing about my blog is that I start receiving lots of interesting research news and articles. Please do send me interesting research. I will try to include them in my post, describe the research and discuss it. You have the benefit that others know about your work and they can give you feedback through comments.

Some days ago, Per Alm has sent me his PhD thesis. He is based at the Dep of Clinical Neuroscience at Lund University in Sweden. He believes in a dysfunction of the basal ganglia as the major cause of PDS: see this article . I didn't have time to read much of his work yet, but the papers look like good science. I like his introduction to history and theories of PDS. Short, clear, and pretty pictures. You can ask him for a copy of his PhD thesis and articles by sending him an email to "Per.Alm AT psychology.lu.se".

In his abstract, he writes: "The theoretical work focused [on] the basal ganglia, leading to a model based on the dual premotor systems hypothesis (G. Goldberg, 1985, 1991), which defines two parallel premotor systems: the medial (basal ganglia + SMA), and the lateral (lateral premotor cortex + cerebellum). Stuttering is suggested to be caused by a disturbance of the medial system, in most cases in the basal ganglia. The core dysfunction is proposed to be impaired "go-signals" from the medial system, supposed to trigger the next motor segment in speech.

Under some conditions speech control is shifted from the medial to the lateral system, thereby bypassing the dysfunction and resulting in fluent speech. The lateral system is suggested to be active when speech is combined with sensory input, like chorus speech or metronome. Also the effect of altered auditory feedback in reducing stuttering is proposed to be based on this mechanism. The lateral system is able control speech timing without sensory input, but this demands increased attention to some particular aspect of speech, as occurs in imitation of dialects, exaggerated rhythm, reduced speech rate, or role play. Also singing is suggested to be based on the lateral system." (Source: Per Alm, PhD thesis 2005, Lund University in Sweden)

It is an interesting theory as it seems to explain the fluency-inducing effects quite naturally. Others also support this theory or at least work on it. Katrin Neuman talks about the basal ganglia in Oxford at the end of this month. And someone else which I don't know called Bijleveld, will talk about the basal ganglia and the limbic system there.

Others are more sceptical, see less evidence and how it should fit the big picture. I will talk about their position in my next post.