This is a threaded discussion page for the International Stuttering Awareness Day Online Conference paper,
Some thoughts on the multidimensional nature of stuttering from a neurophysiological
perspective by Luc De Nil.

The presenter of this paper, Some thoughts on the multidimensional nature of stuttering from a
neurophysiological perspective has consented to have a personal email address posted here if you wish
raise further questions and/or comments. 

Luc DeNil - luc.denil@utoronto.ca 

Multidimensional treatment

From: Ed Feuer
Date: 10/1/98
Time: 3:48:40 PM
Remote Name: 207.161.63.109

Comments

Given the multidimensional nature of stuttering which you describe, would it not make sense to have a
multidisciplinary treatment modity. To make such a treatment system work, a mulidisciplinary team,
coordinated by the SLP and utilizing the knowledge and experience of professionals with relevant expertise as
needed, should be given proper consideration.


Re: Multidimensional treatment

From: Luc De Nil
Date: 10/13/98
Time: 3:39:22 PM
Remote Name: 128.100.47.62

Comments

The multidimensional nature of stuttering implies that assessment and treatment need to identify the various
areas of the individual's experience that need to be addressed in treatment. Whether or not this can be done by
a single individual or needs to involve a number of different professionals, in my opinion, will have to be
determined for each individual client separately. for some clients, working in one dimension will automatically
effect appropriate changes in other dimensions. For instance, working on speech motor skills alone may result
in increased fluency which in turn will result in more normalized personal interactions, will improve linguistic
skills, etc. For other individuals, a particular dimension may be so affected during stuttering history that it
needs specialized help. For instance, if a person who stutters has developed social withdrawal that is so severe
it needs psychiatric intervention, appropriate referrals are in order. Clearly, speech pathologists need to know
when and when not to refer to other professionals. In my opinion, involving a team approach for every single
individual would be an unnecessary waste of money and valuable resources.


Congres in Leuven

From: Gert Reunes
Date: 10/6/98
Time: 1:29:14 PM
Remote Name: 195.238.9.39

Comments

Hi Luc, I hope I will meet you in Leuven the 14th november. Because I will also after my 4 years studying in
Ghent for logopedist go to the USA. Greetings Gert vzw.best@skynet.be


Disfluencies vs. Stuttering

From: Chuck Goldman╩╩╩╩╩╩ chuckig @aol.com
Date: 10/6/98
Time: 5:32:16 PM
Remote Name: 205.188.195.53

Comments

Firstly I have to thank you for a very clear and informative presentation of your view and research findings. In
clinical matters however, is it not almost always productive to view your client via multidimensional models?
If indeed the crux of stuttering lies in the neurophysiological, is it not possible that what is really being
identified is the predilection toward being disfluent rather than the tendency to actually develop a problem that
involves disfluency (i.e. stuttering)In other words we as clinicians and good listeners have met many people
who are disfluent but not stutterers. is it not possible that PET technology has only helped us identify the
tendency to be disfluent. By the way the finding you discovered concerning the differences in silent readers is
most compelling. I'm just not sure you have identified a pathology as opposed to the tendency to have what
could be in most of us normakl disfluencies.


Re: Disfluencies vs. Stuttering

From: Luc De Nil
Date: 10/13/98
Time: 3:48:23 PM
Remote Name: 128.100.47.62

Comments

your comments are well taken. No, we do not know if what we see in the PET scans reflect tendencies
towards disfluencies rather than stuttering. In order to do this, we need to do experiments testing subjects who
are highly disfluent, but not stuttering in the traditional meaning of the word, and compare them to people with
"real" stuttering. Your comments reflect a line of thought in our field that sees stuttering and disfluencies as
being on a single continuum with various degrees of severity. I, personally, am inclined to see stuttering and
disfluencies are categorically distinct, but there is little compelling evidence to back up this view (there's also
not much compelling evidence for the other point of view - just one of those things in our field where beliefs
are still more prominent than facts). 

Regarding your other point, I agree that even if there were a single causal parameter in stuttering, this does not
imply that treatment should not be multidimensional - as I tried to make clear in my paper, you can look at
stuttering at a number of different levels - and for stuttering it seems to make perfect sense to stay at a more
"descriptive level" which allows you to work with your client on aspects that are significant in her or his life,
eventhough they are the result and not the cause of the stuttering problem. 


An inate or early acquired characteristic?

From: Winton Bates
Date: 10/6/98
Time: 11:44:48 PM
Remote Name: 139.134.17.209

Comments

I am interested in your interpretation of the observation that subjects show a different neural activation pattern
during silent reading of single words. I wonder whether this could also be consistent with word phobia ie a
subconscious reaction to particular words resulting from fairly recent experience. 


Re: An inate or early acquired characteristic?

From: Luc De Nil
Date: 10/14/98
Time: 10:51:22 AM
Remote Name: 128.100.204.3

Comments

I think that our own neuroimaging results as well as those reported by others in the past, regardless of
whether they were using brain imaging or electrophysiological data, reflect a combination of acquired and
innate characteristics. In particular the activation observed in the anterior cingulate in our own data seems to be
more conistent with an acquired characteristic following previous experience with disfluencies. I'm not sure I
would go as far as saying that it reflects a phobia, in the psychiatric sense of the word, but we have described
it as possibly representing the anticipatory scanning that so many who stutter experience. It is important to
note that similar cingulate activation is widely reported in the neuroimaging literature, so it is not something
that is very specific for stuttering. 

thanks for your comments 

Luc


disfluent breathing during non-speaking times

From: Susan Logan
Date: 10/8/98
Time: 3:35:11 PM
Remote Name: 207.172.185.155

Comments

Is it common for stutterers to unconsciously hold their breath while doing something like reading a book or
even durig sleep? Is this a more serious form of stuttering - perhaps with a more neurophysiological base?


Re: disfluent breathing during non-speaking times

From: Luc De Nil
Date: 10/14/98
Time: 11:01:06 AM
Remote Name: 128.100.204.3

Comments

I'm not aware of any data suggesting that people who stutter hold their breath more during reading or sleeping
- I guess this probably could be true for individual people. However, it is important to keep in mind that such
behaviour probably is present also in a number of other people who do not have stuttering difficulties. As
such, we have to be careful not to attribute every single characteristic of someone's behaviour as being related
to stuttering. I would think that in the case of holding your breath during sleeping this is probably completely
unrelated to the presence of stuttering.


NEUROPHYSIOLOGY OF STAMMERING

From: jimhoulihan@hotmail.com
Date: 10/16/98
Time: 10:31:22 AM
Remote Name: 194.168.155.209

Comments

Dear Luc I found your article interesting. I am a PWS and did neurophysiology as a major for my first degree.
I am now a patent examiner in pharmaceuticals. I have been quite involved in British Stammering having
chaired a conference for the BSI. From my experience of both anecdotal and scientific I would like to get
involved in creating a model of Stammering. I was thinking, given the information now available, that it might
be an idea to provide an integrated model of the neurophys. and neuropharm. of stammering. For example,
incorporating your mapping work with what's known about neurotransmitters etc. I'd like to get up to speed
on this issue myself. Perhaps if you'd like to email me we could have further discussions. I think your work
is likely to be very valuable. Ultimately do you think localising the involved cortical areas may provide
strategies for circumventing stammering neural networks for us established adult stammerers and for the
redirection of child stammering neural processing. I've discussed all this with my Speech therapist Rosemary
Hayhow whose quite keen on stammering research Regards Jim Houlihan 

Re: NEUROPHYSIOLOGY OF STAMMERING

From: Luc De Nil
Date: 10/19/98
Time: 12:22:05 PM
Remote Name: 128.100.204.3

Comments

Dear Jim, 

thank you for your comments on my paper. I think it would be great if we could put together a neural model
of stuttering, but unfortunately, I think we don't have enough information yet to do this successfully. Mind
you, I'm not one who thinks that we need to have all the pieces of the puzzle before we can try to assemble it.
There is a lot of merit in putting together tentative and incomplete models to help us guide our research. But I
think as of to date we have to many unknowns to even put a tentative model together. For instance, although
there is a lot of evidence of implicate the right hemisphere in stuttering, we do not know what the role of the
RH is. Just stating that it is "less effective" with dealing with the rapid temporal sequences of speech is not
sufficient, because there is a minority of people who control language in the RH and they do not necessarily
start to stutter. Also, patients who undergo a left hemispherectomy can develop near normal speech and
language without stuttering. Just as an example, a second unknown in all of our research is the role of the
cerebellum, which very consistently shows up as being highly activated in stuttering subjects. An additional
problem in all of this is that neurophysiologists in general are still debating what the precise role of the
cerebellum is (is it motor coordination, timing of sensory and cognitive processing, something else ???). I
think that if we can continue to do neuroimaging research, the next few years will start filling some of these
unknowns in stuttering, which, in turn, will allow us to start building working models. These models, in
turn, can then be tested and further refined (or rejected). 

As for the clinical implications, I think that a better understanding of the neural processes involved, indeed,
will allow us to refine our clinical intervention. How this can be done is all very speculative at the present
time, but so is a lot of stuff we do in stuttering anyway. My colleague and I are currently in the process of
trying to formulate a few hypotheses and suggestions, so if you have any ideas, please feel free to share them.
By the way, I don't know where you are in England, but I'm doing a workshop in London (Michael Palin
Centre) on November 16 - if you're there we can discuss this in a bit more detail. 

Neurophysiological basis for stuttering

From: Valerie Johnston
Date: 10/16/98
Time: 2:19:15 PM
Remote Name: 209.30.15.43

Comments

Hello, 

Your paper was very well-written and thought-provoking. I was especially interested in the finding that even
after successful treatment for stuttering and the ability to speak with essentially normal fluency the right
hemisphere bias did not change, but there was additional activity in the left sensorimotor cortex. As you said,
this seems to be very much related to the issue of placticity and may be the reason why it is easier to manage
stuttering in children. On that issue, do you think that the research you and your colleagues are doing now
might eventually give us more information to use when trying to determine which children will outgrow their
stuttering and which will not? 

Again, thanks for a lot to think about. 

Valerie



Re: Neurophysiological basis for stuttering

From: Luc De Nil
Date: 10/19/98
Time: 12:27:39 PM
Remote Name: 128.100.204.3

Comments

Dear Valerie, thank you for your question. I would hope that our growing understanding of the neural basis of
stuttering will ultimately provide some answers as to why certain children seem to outgrow their stuttering,
and others don't. In all honesty, I think that for this we need to look a bit beyond the neural system and also
look at environmental influences which interact with the neural processes. At the present time, we hope that
our neuroimaging research will shed some light on the issue of treatment relapse in adults. An important
question that needs to be answered is to what extent our findings on neural processing also apply to young
children - such research is presently difficult given the technical and ethical restrictions on using neuroimaging
in children. However, I feel very confident that some of the techniques that are currently being developed, as
well as new ones that will undoubtedly emerge in the years to come will allow us to answer such questions.


multidimensional nature of stuttering from neurophysiological
perspective

From: 
Date: 10/19/98
Time: 8:58:48 PM
Remote Name: 198.174.65.202

Comments

How does your perspective of neurophysiological involvement take into account why some stutterers are
completely fluent some of the time, without using learned techniques?

Re: multidimensional nature of stuttering from
neurophysiological...

From: Luc De Nil
Date: 10/22/98
Time: 12:41:43 PM
Remote Name: 128.100.47.62

Comments

dear anonymous, 

indeed, many people who stutter will attest to the fact that they are stuttering sometime (or often), but not all of
the time. Such an observation does not contradict a neurophysiological basis of stuttering. Indeed, there are
many exemples of other disorders that only intermittently affect people - a good example is Tourette's
syndrome. Tics do not occur all the time and the frequency of the tics often is influenced by the situation (from
none at all to often). Nevertheless, few people would argue that Tourette does not have a neurological basis.
Secondly, saying that stuttering has a neurological basis does not imply that environmental influences do not
play a role. On the contrary. Environmental factors can play an important role in whether stuttering occurs or
not, and how severe. It is a general misconception that stating that something has a neurological (or genetic)
basis means that the behaviour under investigation has to occur all the time, or can not be influenced by
environmental factors. 


ongelooflijk

From: Gert reunes
Date: 10/21/98
Time: 9:02:25 AM
Remote Name: 195.238.9.6

Comments

Beste Luc, Wat is de wereld toch klein. Ik mailde jou zonder te weten dat jij Luc bent die nog therapie aan mij
gegeven hebt... Eergisteren belde ik de Dhr VanKerckhoven en die melde mij dat jij inderdaad nog werkte in
Gent op het revalidatiecentrum... Luc, het is voor mij dan ook zeer belangrijk om jou toch eens te ontmoeten.
Ik zit nu in mijn 1ste licentie logopedie aan de RUG als ik wil stotter ik niet meer en dat sinds 4 jaar. Ik ben
ook bezig met een boek de mens achter de stotteraar. Ik heb zovele projekten en ben dus ook bezig met de
wereldstotterdag in BelgiĹ waar ik coÜrdianator van ben. Indien je in Gent zou zitten kom gerust af en ik betaal
je een pintje :-) 

vele groeten en cu 

Gert 


Re: ongelooflijk

From: Luc De Nil
Date: 10/22/98
Time: 12:52:56 PM
Remote Name: 128.100.47.62

Comments

To all, this is a response to a personal message I received from someone in Belgium. I reply via this route
because I do not have his personal email. I apologize for those who can not read Dutch, but rest assured that
nothing professional is discussed. 

Best Gert, 

inderdaad, de wereld is klein - toen ik je naam zag kwam die mij al bekend voor. Het is fantastisch te
vernemen dat je ondertussen zelf ook aan logopedie begonnen bent en nog zo actief bezig bent met de
stotterproblematiek. Jammer genoeg ben ik maar een paar dagen in Belgie (ik reis na de conferentie af naar
London waar ik ook een workshop geef op maandag en daarna is het naar Texas voor andere presentaties).
Naar Gent komen zal er jammer genoeg niet inzitten, maar indien je in Leuven bent wil ik je graag opnemen op
het aanbod om een pint te gaan pakken. 

groetjes, 

Luc

DAF

From: Gert Reunes
Date: 10/21/98
Time: 9:17:32 AM
Remote Name: 195.238.9.6

Comments

Hi Luc, What is your opinion about the use of DAF equipments...??? I know that in Belgium there is no
support for such systems. I believe that there is a need to use this devices because what do you do with people
with real severe stuttering behavior??? On my own experiences I had very good results with this DAF device.
I think that the auditory loop is disturbed because when i use the hausdÜrfer methode i speak fluently, when I
use the DAF i speak fluently . I hope that I can do some research on this case. I was already in contact with Dr
Kalinowski and casa futura. Next month I will have a meeting with dhr Jo Lernout from Lernout and Hauspie
because such devices costs here in belgium 70.000 Bef and I would like to make it in a software program. It is
true that use of devices not always gives results but for real stutterers it is like dope for a drugaddict. 

My professor Van Borsel UZ Gent is standing behind the project. So perhaps i will re-invent the use of
DAF... 

Greetings Gert 22 nd october auditorium D tussen polikliniek 3 & 4 UZ GENT 14u deel 1 voor studenten
logopedie en logopedisten 19u30 deel 2 voor stotteraars en leerkrachten lager onderwijs en kleuteronderwijs 



Re: DAF

From: Luc De Nil
Date: 10/22/98
Time: 12:58:55 PM
Remote Name: 128.100.47.62

Comments

Dear Gert, 

thanks for your comments. I'm not sure where DAF fits in in all of this. Clearly, when providing delayed
feedback the speaker is provided with a very distorted signal of his own speech compared to normal feedback
signals. It would be very interesting to investigate what changes take place at the neural level under DAF. This
might shed some light on the actual compensation processes that are taking place. Clearly, DAF works from
some people, even if it is only temporarily. As such, it's potential use in treatment can not be ignored. As with
everything else, it boils down to differential diagnosis and treatment - what works for one does not necessarily
work for someone else. The real challenge for researchers is to try to find out why. Good luck on your
project!



Model of Stuttering That May Explain Some of Your Findings.

From: Darrell Dodge
Date: 10/22/98
Time: 2:00:25 AM
Remote Name: 152.167.141.177

Comments

Dear Luc De Nil: 

Happy Stuttering Awareness Day. 

Thank you for a most interesting review of your recent findings. I agree that the basis of stuttering is
neuro-physiological or neuro-psychological (take your pick) and would like to propose for your consideration
a theoretic model of stuttering that helps explain some of your results. My reason for writing is frustration that
you and other researchers continue to look in the cortical regions for something that will explain the cause and
trigger of stuttering, as if stuttering is primarily a language, cognitive, or executive function. In fact, given the
observable lack of language, cognition, or executive impairments in many people who stutter (other than the
predictable effects of speech disruption), there is every reason to suspect that stuttering is triggered
somewhere else. 

As you note in a response elsewhere on your conference page, investigation of RH function or dysfunction
yields very little that is relevant to stuttering because such dysfunction is present in many other people (victims
of stroke and trauma, etc.) who do not stutter. Other investigators who are toying with concepts such as
insufficient dopamine re-uptake have similar problems. In the later case, imbalances of dopamine (up or
down) are associated with schizophrenia and Parkinsonism, two disorders that do not link with stuttering in
any plausible way. Excesses of dopamine are also associated with Tourette syndrome, but this is a disorder
the symptoms of which can be virtually stopped with drugs - the same drugs that are only effective to the level
of placebo (or less) with stuttering. Apparently, no one is really considering the possibility that all of these are
residual or secondary effects of another - more basic and plausible - process. 

The brain activity patterns you describe are completely consistent with a theory of stuttering that views the key
factor of the disorder as an involuntary but active inhibition of speech, similar to a "freeze" response, which is
based in subcortical survival responses and becomes deeply and permanently reinforced through classical
conditioning. Given the observed characteristics of stuttering and its association with hormonal, auditory, and
other cues, this involuntary response would seem to become automatic given the presence of appropriate cues
during the later stages of development. Among the key brain areas targeted by such an inhibitory response
would be neurons projecting from subcortical areas such as the amygdala to the basal ganglia and thence
directly or indirectly to the left primary and supplementary motor cortex. Other areas would be the more
"vegetative" neurons of the brain stem that project to the larynx and other peripheral structures and have
important roles in survival and preservation responses. Of course, there are the voluntary (secondary)
behaviors as well, which are associated with attempts to overcome or control the inhibitory response (which is
perceived internally in various ways by the person who stutters) and can become habitual. And the severity of
the reactive response in different individuals would be largely subject to genetic factors. The anatomical basis
of such reactivity in the amygdala and associated structures in the so-called "limbic system" or "Papez circuit"
has been very well described by LeDoux and other researchers who have begun their explorations by
examining the survival aspects of fear. And the independent (pre-cortical) monitoring of auditory input by the
amygdala provides an explanation for the close association of auditory feedback with stuttering, including its
extinguishment with DAF, which delays the perception of most auditory feedback until after the speech
initiation process for the relevant sound is completed. 

The subcortical source of such inhibitory activity would not necessarily show up on PET scans because it
involves of necessity a relatively small number of neurons (one of the weaknesses of PET scans in diagnosis).
An overlay of cortical activity (predicted by the theory) that involves the inhibition of the core inhibitory
activity following successful speech therapy may also be evident in your scans. (It also may be showing up in
recent EEG measurements at East Carolina by Kalinowski.) Of course, as you note (in another way),
conditioned neurological reactions based in the amygdala are indelible at the level of the affected neurons,
although they can be extinguished at the higher level of speech motor planning and activation through the
overlaid (or invasive) cortical inhibitory processes (inhibition of inhibitions). The clinical course of stuttering
therapy -- which you are very good at describing and understanding -- is one of the things that tends to
convince me that an active inhibition theory of stuttering is plausible. A very readable explanation of how such
a system would work from a basic developmental and clinical perspective is provided in the new material in
the latest edition of the classic text by Barry Guitar. I can lead you to additional (and more speculative)
information sources if you're interested, including my original formulation of this model in 1995. 

There is nothing really new in the inhibitory therapy of stuttering discussed above. It is simply the
consequence of my "reverse engineering" of the conviction of many clinicians and researchers that the
development of stuttering is primarily driven by reactions to initial childhood disfluencies or (in some cases)
stressors associated with expressive language difficulties, and that these reactions are subject to conditioned
neurological learning processes that become virtually permanent with time. There is a large body of research in
the areas of survival responses and conditioned emotional responses that is already in place for all of us to
explore. Somehow the connection between the theory and the bulk of current experimental research (which is
in brain imaging of various types) is not being made. I suspect this is partly because the imaging guys (like
you) may not be talking to the experimental psychologists (like LeDoux) who can explain the underlying
processes. 

At the same time, it is a bit troubling to read your statement that any model of brain neural functioning can be
proven or dis-proven based on neuroimaging. As I understand it, the jury is still out on the actual usefulness
of such imaging in research involving underlying brain processes. 

Thanks again for your interesting and stimulating article. - Regards, Darrell Dodge. 


Re: Model of Stuttering That May Explain Some of Your
Findings.

From: Luc De Nil
Date: 10/23/98
Time: 11:55:00 AM
Remote Name: 128.100.204.3

Comments

Hi Darrell, thank you for the lengthy and detailed comments on my paper. I want to provide a few comments
of my own before the electronic conference is closed. These responses will be brief but I hope to have the
opportunity at some point in the future to discuss them in more detail in some other forum. 

1. I did not mean to imply that studying the RH will not reveal important information about stuttering. What I
wanted to explain in the paper is that merely talking about RH involvement in speech production does not
explain the phenomenon of stuttering. Indeed, as you too point out, not everyone who has to rely on the RH
for speech and language will stutter. If the RH is involved in the onset and development of stuttering, it is my
belief that we will need to do a better job at differentiating the various (sub)processes that take place within the
RH and try to relate these to stuttering. Let me give two hypothetical examples of what could be happening: 1.
people who stutter (like some other nonstuttering speakers) rely on RH processing for some aspects of
language formulation, but while the more cognitive processes (thought formulation) take place appropriately,
for some reason or another, they experience difficulties within the RH with the motor coordination resulting in
stuttering - in this example, a deficit in the RH is "to blame"; 2. everyone uses both left and right hemispheric
processes during language formulation (that is a proven fact), but people who stutter experience a deficit in the
LH processes for motor coordination. The RH tries its best to take over this task, but is unable to do this
effectively resulting in stuttering. In the latter example, the deficit in the LH is "to blame". In both examples,
however, studying the processes that take place within the RH can be very informative about the nature of
stuttering. 

2. your hypothesis about the role of the amygdala in stuttering is very interesting. But as with every other
model, it needs to be tested in one way or another. I have seen no evidence in any of the neuroimaging studies
of increased or decreased activation in that area. That of course does not mean that the amygdala is not
involved - only that it has not been observed to be active. Contrary to what you state, the amygdale can and
has been observed in neuroimaging studies in humans. I am aware of Ledoux's work in the area of emotions
and I think it offers a number of intriguing questions that await experimental testing. The question, of course,
always remains, why does it affect only some children and not others. Referring to environmental triggers in
my opinion, does not explain anything because many children experience identical or very similar triggers and
do not start to stutter. So there must be something that is very specific to the brains of children that determines
how these triggers are processed - and that is exactly what we are trying to answer in our studies. 

3. I certainly do not see the current functional neuroimaging techniques as the ultimate method to test
theoretical models. As a matter of fact, I have stated repeatedly in publications and presentations that is a very
good tool, but only a tool. It will answer certain questions and not be able to answer others. If we want to
understand the workings of the brain, especially when we are looking at models that hypothesize about
processes at the millisecond level, it is unable to do so and PET or fMRI need to be combined with other
methods, such as electrophysiology. In other words, neuroimaging will help us find the answers, but it would
be a bit naive considering the history of the study of the human brain that it will prove to be able to give us all,
or even most of the answers. If I implied otherwise in my paper, I apologize for the error. 

thanks again for your thought provoking response