Blog background



I have been deeply involved in sharing my understanding with fellow stutterers, speech and language pathologists and researchers, especially in the 90's. The older part of this blog reports some the discussions I was having on a professional list at that time. Most of the discussions are still relevant today.

I remained involved in the stuttering community, mostly as participant in activities of the National Stuttering Association (NSA), and occasional workshop leader. Since my retirement I have returned to writing, and I just developed an audio course on fluency improvement. A link for the course can be found in this blog, as well as posts based on more recent discussions I am having in a Stuttering Facebook group.

Wednesday, January 25, 1995

Model-1

To M. Schwartz

> We have gone around in one big loop. In an earlier message you
> described three apparently seperate "theories" of stuttering (organic
> based, tension based and learning based), then made the following statement:
>
> > > "So, as you can see, all three theories are correct and all have their
> > > appropriate place in the model"
> > >
>
> To this I replied the following
> >
> >
> > Indeed I think all three "theories" are "correct" i.e. they cover
> > likely important aspects of the stuttering phenomenon, but I fail
> > to see how your model is a particularly parsimonious way to account
> > for them.
> >
> > An organic weakness can easily make someone more vulnerable to
> > tension (some people blush instead of stuttering - my palms sweat...AND
> > I (used to) stutter under tension). In addition, when faced with
> > difficulties, we learn behaviors that seem to help us overcome them.
> > Sometimes these behaviors end up being worse than the problem. Persons
> > who blush may cover their faces with their hands, which may end up
> > being more noticeable than the blushing...
> >
> > In this context one can have therapies that work at decreasing tension,
> > unlearning unproductive behaviors and/or learning good ones, and, if
> > a good drug is found, the "root" organic problem might be addressed
> > as well (too much or too little seratonen...or what have you).
> >
>
>
This simple explanation of how these ideas can easily be combined in
> providing a rough accounting of stuttering behavior is what I called
> "model 1" ... just as a reference point. I make no claims of having
> created or proposed a model that is "mine". Model-1, it seems to
> me, (please SLPs correct me if I am wrong) underlies most therapeutic
> efforts in stuttering.
>
> My question to you was and is very simple: are there stuttering behaviours
> which can be accounted for ONLY by your model and not by this
> reference model (Model-1)? I really would like to understand.
>

No comments: