Monday, February 13, 2012

Why Stutter Happens

I've been mulling some ideas over, and I find that the best way to clear my own mind is to put words on a page. Here, I'd like to speculate on why we stutter, and why we stutter when we do. In this case, my question does not refer to ultimate causes, such as a possible mis-wiring in the brain, or proximate causes, like a learned anxiety over saying one's own name. I'm looking to a level of cause somewhere in between the two extremes.

I'll start with the observation that slowing down speech decreases the occurrence of stutter blocks, and a dramatic slowdown can eliminate them. So I'll take it that a certain rate of speech can trigger stutter blocks. Much research has looked at the origin of blocks. Linguistic sources have been examined (the accessing of words from memory) as well as motor plan failures (the instructions to carry out coordinated muscle movements to generate words).

Rather than choosing among theoretically possible sources of the error and explore them, I prefer to start from what I know. When stutter blocks occur (at least in chronic, adult stage stutterers), they typically occur as failures of coarticulation within syllables. Whatever the nature of the original failure, the basic pathology of stutter is this temporary loss of the ability to coarticulate phonemes (sounds) within a syllable.

Whatever the neurological origin of the stutter block, or the psycho-social trigger that cues it to occur, we know two things: that the failure is a failure of coarticulation, and that the failure doesn't occur when the rate of speech is slowed down sufficiently. So what can we do with these two facts?

First, we need to examine the process of coarticulation. In generating syllables and words out of individual sounds, human speech does not simply connect the sounds in sequence, like beads on a string. The articulation of an initial sound will be modified by putting the articulators (lips, tongue, jaw) in position to immediately generate the following sound. My example from a previous entry was Seesaw (or See-Saw). When the speaker begins to produce the 's' sound in the syllable 'See,'the articulators are already in place to produce the 'ee' sound. The 's' and 'e' sounds are not produced through independent actions - they have become a single, simplified unit. The same is true in the production of the syllable 'saw.'

Coarticulation allows us to speak significantly faster than independent, sequential production of individual sounds would allow. We can imagine how this might have been important to our ancient ancestors on the African plains. The ability to transmit the information "Hey, Nog, there's a lion in the grass right behind you!" would be critical to the survival of the individual and the family group. Somewhere along the line, human speech was turbo-charged by this sound-blending, articulation-modifying process.

In speeding speech, coarticulation also puts stress on the rest of the speech production process. Words must be accessed faster, and proper grammatical structures built at the same time. While the average rate of speech measured by syllables per second varies somewhat across languages, the differences are not great. Speech production is a complicated, rapid process, like nothing else we do until we take up musical instruments and practice many years.

Native English speakers have been determined to average in the 5-6 syllable per second range. If we take 5 syllables per second as a working number, we have each syllable taking an average of a fifth of a second to produce. But this is an average summed over many sentences. When we look closer, we see that if we account for pauses between sentences, the rate within sentences would actually be slightly higher. And we need to account for the fact that multi-syllabic words are spoken faster than mono-syllabic words. In the sentence "She's a beautiful girl," the three syllable word 'beautiful' is spoken in approximately the same time as 'girl.' So while an average gives us a useful approximation of syllable rate, in actual performance some sequential syllables are generated faster than others.

Within syllables that are produced sequentially in a fifth of a second or faster, the coarticulation process must not only produce multiple sounds, but must modify the motor plan for producing them into new, hybrid forms. Without training in speech science, this seems to me to be the most difficult part of speech production to execute.

So the answer to the question 'why does stuttering happen?' would be because coarticulation happens at the most rapid time-scale of all speech processes. Thus, it is the weakest link in the speech production process, and the most likely to fail at normal (rapid) speech rates. And rate-controlled slow speech sees the elimination of stutter blocks because it relieves the break-neck speed requirement of the normal speech process. That's speculation through and through, but speculation based on a reasoned examination of what we know.

One puzzle is that while adults tend to block more during (longer) content words, children beginning to stutter are reported to block more on (shorter) function words. One explanation for this difference is that children might block on the word before the longer content word that is actually triggering the block. This is possible, but if this tendency of early stutterers to block on short, often single-syllable words is correct, then it tends to go against my proposal. For now, I'll leave it up in the air as merely a thought-provoking suggestion.

Friday, February 3, 2012

Why 'Neurogenic' Matters

Commenter Ora was kind enough to make a thoughtful response to my last post on why 'neurogenic' and 'developmental' stuttering are not are not good complementary names for the two related conditions. This raises a classic blogging issue - with no editor to pre-read and review copy, a writer can never be sure that the intended message is getting through. I know what I think, and I know what I want to say, but I can't know that I'm writing well enough to make my point.

My previous post on the use of the term 'neurogenic' was intended to be short, as a respite to my usual long-winded (blog-wise) entries. Let me take the opportunity to elaborate on the important reasons why I think it's worth making the neurogenic distinction.

First, regardless of the importance of learned behavior in the confirmed developmental stutterer, the condition of developmental stutter either is or is not of neurogenic origin. I happen to believe that the evidence, both direct and indirect, is sufficiently strong to favor a neurogenic origin as a default assumption. If this is true, then the term neurogenic cannot logically be used to distinguish the developmental and acquired versions of the condition. Even if one is not fully convinced that developmental stutter is always neurogenic in origin, there is sufficient evidence pointing in that direction to make the developmental/neurological distinction a poor one for distinguishing the two types of stutter.

When a child starts to show signs of stuttering, an obvious question is 'why?' What is causing the disordering of the child's speech? For decades, many believed that children naturally spoke imperfectly, and gradually 'learned' to stutter. This was always an assertion, rather than a theory or even hypothesis, and it was wrong. The weight of evidence favors the belief that children start to stutter during their speech development process because they have a neurological deficit of some kind. Whatever happens later in life, the beginning stutterer has a neurological condition, and retains that condition as long as they stutter. That there are learned elements to chronic stuttering is certainly true. However, if one were to strip away the learned behaviors (eye blinks, head jerks, forced articulation, improper breathing, etc) from the basic neurological element - the block - what would we be left with? My answer is: a stutterer. Thus, there is the (neurological) condition - stutter - and there are the behavioral and affective responses. Should a condition be defined by its fundamental nature, or by the response to it?

A particular (and practical) motivation for my emphasis on the neurological basis of developmental stutter is the support such an understanding could give to stutterers themselves. For any stutterer, the knowledge that their condition has a specific, organic source rather than just 'something that happens' could be a comfort when dealing with it. Based on Internet stutter groups, many stutterers don't have the slightest knowledge of the condition, and old wives tales are as common as science among the afflicted. When you have people insisting that 'you can catch it,' we shouldn't be surprised that so many stutterers have difficulty dealing with the condition.

A specific case for the value of defining developmental stutter as neurogenic would be in cases of therapeutic relapse. Stutterers who go through stutter-suppressing therapy like fluency shaping can find that a relapse leaves them worse than when they started therapy. This can induce guilt and depression over the lost 'fluency. If one started with the understanding that developmental stutter has a neurogenic basis, it would be easier to accept the possibility of relapse. Under the neurogenic assumption, stutter therapy is an attempt to 'fight city hall.' If we are trying to fight the wiring of our brains, rather than 'bad behavior,' then we can understand why it should be so difficult to eliminate stutter blocks entirely.
A stutterer grounded by an understanding of the neurogenic basis of the condition should be less likely to experience such high highs (assuming their stuttering is 'cured'), and low lows (crashing and burning after relapse).

To commenter Ora's point about therapy: by it's nature, all stutter therapy must be behavioral. Drugs have been tried, and found wanting. We can't get at the brain, so we can only make conscious efforts to modify speech. I don't think there's any fear of taking away from this necessity by stressing the neurological basis of the condition. Until there is some fundamental breakthrough in treatment, stutter therapy can only involve three elements; cognitive, affective and behavioral. That is, we can learn about the condition, we can learn about how the condition affects us emotionally, and we can learn to modify the actual speech process. My stress on the neurogenic basis of stutter is part of the cognitive element. Alone, it does nothing to change speech. It could, however, serve the therapeutic process by setting parameters. Stutter is not a behavioral bad habit, simply to be unlearned. The learning process of stutter therapy is a process of actively learning to deal with the neurological element - the block. To me, this is the critical issue of stutter therapy. The piano student must master the challenge of difficult finger movement and coordination. But for all the difficulty of mastering the piano, the piano does not fight back. The neurological abnormality that triggers the stutter block does. One doesn't practice a away stutter and become a normal speaker - at least very few do.

Although most stutter therapy doesn't actively raise the neurological issue, most deal with it implicitly. The fluency shaping approach doesn't explicitly rule out a neurological basis for stutter, but it does work on the assumption that either there is no such basis, or that it can be over-ridden through training. The stutter modification school of therapy isn't based on a neurological theory, but it provides pragmatic treatment as if it did. Both schools of therapy engage in behavioral therapy, but the two are very different in outlook and in practice. By insisting on bringing out in the open the biological nature of the condition, we implicitly demand that different schools of therapy justify themselves to the facts of the condition.