Wednesday, October 16, 1996

More on the radical neurological position

Marty Jezer stated that "the core neurological problem is not a singular problem. There is no one stuttering circuit that governs stuttering/fluency (just as there is no one gene that causes stuttering"

Marty:

You could be right, but does it hurt to think of one core cause for a start? Let's look for the most likely ONE... and if doesn't do the trick let's look for more (..Occam's razor). The issue of speech circuits and genetics are related, but different. Genes are simply "switches" that set a whole development process in motion. In this context I would also bet against a "single gene" for stuttering. But suppose the problem is simply caused by low levels of some chemical whose production is dictated by a
particular gene... It may be unlikely, but not entirely implausible.

I don't think nature would create a "circuit" for stuttering, but, given a well developed and honed circuit for speech, there could be a particular weak link, such that, if anything is going to break, that's the link that's going to break. As part of my job, we flew one of the early Apple Powerbooks on the Shuttle. With all its complex circuitry, there was one fuse that had a tendency to blow up for no apparent reason. We were lucky - it didn't break - but we were sweating it (BTW, no danger to people.. only to an experiment!)

Mary continues:
> Speech, being as complex as it is, is subject to
> many areas of vulnerability, and many different singular and
> interactive neurological glitches.

Again, we really don't know. Some symptoms (sneezing, for example) can have multiple different causes (dust, allergies, colds etc.) and some have a clear specific cause. Complexity, in and of itself, doesn't imply several equiprobable failure modes. The heart keeps on going and going. The most common serious mishap is a heart attack ... and then the symptoms are clear. You could be right, but let's not use the "multiple glitches" possibility as an excuse to throw our hands up in desperation. Give me "one" glitch ... and the others will follow..

Marty also stated that drug research isn't really looking for a "fluency pill", rather for a pill that might lessen brain excitation and thus "affect the threshold of motor malfunction"

Some drugs can cure causes, some can cover symptoms. If the latter is the
best we can do, I'll take it!



Woody Starkweather stated his objection to the "radical neurologial" position on the grounds that, once the onion is peeled (using my metaphor), there is virtually no problem left.. just some "behavioral residue" so small that it is not likely to be the result of some neurological flaw.

You stated the objection and then you actually answered it. I've personally been stuck with this possible "behavioral residue" for a long time. The reason why I remain somewhat active in the stuttering community is no longer the need to find a cure for myself. Stuttering has stopped being an issue for me. I just feel that this "behavioral residue" is the KEY to the problem. From a therapist's point of view, the problem has practically vanished. I think that this is the point where one can finally start addressing and studying the real problem (from a researcher's point of view). The point is not that we need to push the "cure" further (although I wouldn't mind) but that understanding the core problem could prevent in the future the accumulation of all the upper layers.

Another "perverse" reason why there isn't much left after peeling away at the layers *could be* that the layers allowed themselves to be peeled away only because the core cause abated. Just like most children become fluent after "stuttering" periods, possibly aging, in some adults, also affects a "cure". I have mentioned this several times and I am surprised that this possibility hasn't been looked into (that I know... do set me straight). Let's study "recovered" stutterers!

Let me also mention that I must concede that between your emphasis on early intervention and "core neurology" there may be only a semantic difference. As we have discussed in the past, it is often impossible to differentiate soft from hard circuitry in the brain.. and when one turns into the other, and if and what effects the early environment has on this process. If presumably the core problem is "structural" I have no strong arguments for stating that this faulty structure had to be present at birth as opposed to say after 2 or 3 years of childhood development.

Do we start with a only very vague predisposition whose "hardening" could almost always be avoided (with the right care), or do we start with a predisposition whose hardening is usually inevitable? From fetus to the first few years we must understand what we can do and when. I consider your work well within these very important parameters.

Thank you!!! (And thanks also to all the therapist who work at the "upper layers" to relieve so much pain and to help make us functional..)

Sorry about this long post, but everybody had been making such good
points that I couldn't resist packaging it all together.

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