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An “Elevator Speech” for Stuttering

With the discovery and recent verification, over the past 10-12 years, of neurological correlates for childhood stuttering in 1) white matter fiber tracts from premotor planning and linguistic areas of the left hemisphere (Chang 2009, etc.) and 2) genetic lysosomal disorders in neurons (waste processing systems) (Drayna, NIH), it is possible to predict emotional reactions associated with delays or errors in required inputs for speech to the “go” and “no-go” systems at the basal ganglia.

Thus, the following prospective “elevator speech” is possible for the long-sought cause of stuttering:

“Stuttering behavior is caused by emotional reactions to timing delays and errors in the neurological speech system, which become fear-conditioned over time.”


Yes, Alan Turing Did Stutter

Despite appearances to the contrary in the film The Imitation Game, the latest of several bio-films and plays about Alan Turing, the brilliant mathematician and computer pioneer did have a quite-noticeable stutter much of the time. How do I know? Because I saw a film of him lecturing that was spooled at the computer exhibit in the Smithsonian in the early 1990’s. The film was a segment of a lecture on the general operation of  computers and the possibilities of computers to assist mankind. It was clearly aimed at a general audience (probably the reason it was selected for display at the Smithsonian.) His stutter was what I would call “stuttery,” as he was able to move forward through the speech quite well, and was quite unaffected by secondary behaviors. But his disfluencies were continuous and interesting enough to me that I watched the film clip for 15 or 20 minutes. His sister is apparently quoted in her biography of  Turing as saying that the stuttering was “painful,” (which often means that it is painful to listeners.) An adult friend of Turing’s is quoted in that book as saying that “Alan had the most uninhibited stammer I have ever heard,” perhaps indicating that Turing had worked through his reactions to stuttering to the point that it just wasn’t a problem anymore; or had become so unconscious of it that he really didn’t notice it while he was speaking (which may be the same thing!)

Below is a YouTube video of Benedict Cumberbatch (that I found on the great Canadian Stuttering Association Web site) explaining how he prepared to play the role of Turing and how Turing’s stuttering was regulated to reduce its importance in the film, (and reduce the “jangling” distraction that would be introduced by stuttering) except for moments when Turing was under stress. The possibility that Turing may have actually stuttered less when he was stressed out or angry probably never occurred to the filmmakers. In the clip, Mr. Cumberbatch refers to an “audio” that the movie-makers tried to locate but was somehow missing. I suspect that may have been the one I watched at the Smithsonian — which may even still be displayed there.

I was frankly quite disappointed that a bit more of Turing’s stuttering was not included in the film. Though I was mightily impressed by Mr. Cumberbatch’s acting, this omission adds another historical inaccuracy to a film script that is filled with inaccuracies.  As it is, the film falls prey to the myth that stuttering is caused by nervousness or anxiety, and this results in yet another disservice to people who stutter.

Thank you to the Canadian Stuttering Association for the source article.

Stuttering Genetics and the Hippocampus

In my last long-ago post, I brought up the fact that the recent NIH study of stuttering genetics suggested that mutations in 3 genes associated with stuttering in 9% of people who stutter were expressed in the mammalian hippocampus, a brain structure not commonly associated with speech.

How can that be?

To date, all of the genetic mutations found to be associated with stuttering are in the lysosomal system of the cell. The is the so-called “housekeeping” system, where the mutation causes the wrong protein to be generated, resulting in lowered efficiency of the cell due to the buildup of waste products. Because the hippocampus is one of the primary areas of the brain that is associated with memory, proprioception (spacial and motor movement awareness), and emotion, virtually all higher brain functions rely on the prompt completion of its actions to work properly. Lagging or inaccurate response by the hippocampus could contribute to the minor sorts of motor “glitches” that are thought to be associated with beginning stuttering. The close association of the hippocampus with the amygdala in the production of emotional memories might play some role as well.

Videos That Depict External and Internal Inhibition of Speech

I came across two interesting videos on YouTube today that show overt manifestations of the inhibition of speech that accompanies stuttering behavior.

The first shows the response of a fluent person’s speech to a magnetic pulse applied to his left brain hemisphere that disables the speech mechanism (causing eye flickering and stuttering-like speech) and then shows the man singing right through a similar magnetic pulse as he uses his right brain to sing.


The second shows a delightful woman whose handle is Spazzyme, as she as responds with eye-flickering and temporary loss of consciousness to the disabling of her speech mechanism by an active inhibition or freezing brought about by fear conditioning. It also shows her using a fluency-enhancing stretch or voice softening to avoid/inhibit a stutter on a /w/

Spazzyme – from YouTube

Note that while the responses are overtly somewhat similar, there are very different processes that are causing the stuttering and stuttering-like behaviors.

The King’s Speech: Looking Back at An Initial Take

What follows is an old blog that never got posted, offered for what it’s worth:

Finally got to see The King’s Speech at its opening here in Denver, 12:45 pm on Christmas Day.

Some initial observations:

1. The production is impressive; actors are immersed in their roles; the King’s stuttering is well done by Colin Firth, who also accurately reproduces the worried look of some adult PWS; soundtrack is non-intrusive; all of this creates the uncanny sense of what we identify as “cinematic” reality. 

2. The King’s therapy objectives are to not stutter, especially while reading speeches for live and radio audiences.

3. The clinician (Lionel Logue) respects the client’s wishes and develops a voice/speech motor treatment program designed to do that. This program ( once the King allows) is augmented with some psychological counseling to help build the client’s confidence. Many of the “therapy techniques” turn out to be fluency tricks or stunts rather than activities that would more directly assist in providing the deconditioning required to facilitate the process of stuttering recovery. The primary transfer technique is oral reading in a many that would be described as “chunking and voicing with relaxed pauses;” great for oratory but difficult to use if one doesn’t have the automatic deference provided to a king.

4. The King is successful in learning how to hide his stuttering in public, though he requires the presence of his therapist to coach him through his speeches. It is not clearly explained in the film that the elapsed time between the beginning of the King’s therapy and the triumphant conclusion was more than 10 years.

5. The result of therapy is that the King can put on a credible show of fluency and strength for the British people to maintain civic pride and help them get through the Second World War.

Based on these observations, I don’t personally see how anyone could hope to use this film either as an accurate portrayal of modern stuttering therapy or as a forum to present the complex modern theories about the cause of stuttering in a way that modern viewers of the film can understand. At the same time, the reviews of the film that allude to the “cure” or “overcoming” of the King’s stuttering are totally unsupported, even by the standards of the period the film portrays.

On the positive side, the film demonstrates the frustrating nature of stuttering for the person who stutters, and may even inspire people who have been avoiding stuttering therapy to give it a try. It will offer a chance to educate the public about stuttering by providing a foil with which to compare the real struggle of stuttering and describe modern stuttering therapy approaches, including stuttering modification, acceptance of stuttering and voluntary stuttering.

Reason for Hope (Outside the Box)

In the last episode, I discussed how the authors of a paper on the neurology of stuttering were trying to use a model of normal speech control created by Jurgens to describe and explain stuttered speech. This led to the authors concluding that stuttering was primarily caused by brain “structural and functional abnormalities,” (disordered cerebral dominance seemed to be favored) while granting that there may be “psychological” and “emotional”  factors that may be treated. According to the authors, the “most exciting explanation” was a theory of “delayed cerebral maturation” proposed by Ozge (2004), (a not-very-promising cul de sac.)

So, why is the Jurgens model important?  Simply that it’s being used to guide a lot of stuttering research efforts, in particular, brain scanning studies.

Meanwhile, on the edges of Jurgens’ box are some very important systems and structures that the authors virtually ignore in their conclusions, including 1) auditory input, 2) proprioceptive input, 3) the anterior cingulate cortex, and 4) the periaqueductal gray (PAG). These are all elements of speech generation that are capable of transmitting disruptive or inhibitive inputs from the brains emotional/attention system to the speech system that comprises the Jurgens model. In fact, Jurgens himself discussed these elements in a presentation to the NIH which raised the (apparently, long forgotten) possibility that the amygdala, hippocampus, PAG, and anterior cingulate cortex are importantly involved in stuttered speech.

(This is not to say that the speech system of people who stutter (the “box”) is free from defects. It’s just that the violent nature of a lot of stuttering behavior is difficult to square with the relatively minor differences in the neurological performance of PWS when they are not stuttering, or those who are in recovery — without brain surgery, gene therapy, drugs, or stuttering inhibition aides.  Or the lack of significant differences in many other activities.)

The stuttering research community steadfastly refuses to acknowledge that emotion is not a peripheral concern when it comes to stuttering, but is an integral part of the disorder.  Indeed, since emotion is — in the broadest sense — a system for warning life forms the something is wrong and needs to be attended to, it can be argued that the reaction to speech disruption (i.e., stuttering) IS ITSELF an emotion.

This refusal has resulted in the inability of stuttering researchers to actually address the disorder. Instead, we have scores of papers characterising stuttering behavior by comparing it to fluent speech; earnest research efforts to analyze the types of words, phrases,  and sentences that people might stutter on; quasi-phrenological studies of the shapes of brains of people who stutter; and tautological brain scan research that concludes: “that brain is sure not working properly when he stutters!”

Fortunately, there is reason for hope. At the conclusion of Dr. Dennis Drayna’s recently published talk on his team’s recent discovery of three gene mutations associated with stuttering, he notes that an analysis of gene expression for the resulting lysosomal mutations fingered the hippocampus.

The hippocampus, a brain structure that is not usually thought of as part of the “speech system,” but is part of a circuit associated with conditioning, emotional memories (particularly of places and situations), proprioceptive awareness, and epileptic seizures and motoric freezing, among a host of other behaviors.

(Revised  7/1/2010)

Stuttering Inside the Box

Long time since I blogged here, probably because I need to blog shorter!

Sometimes, things are so obvious that they’re difficult to see. I was looking over the Jurgens model of speech production, which has been used as a road map to guide thinking about speech control since it was published in 2002, wondering why it didn’t include any mention of the amygdala (which readers of VOS know is said by me to be an important element of a brain circuit involved in stuttering reactivity). Jurgens included a lot of important information about the amygdala in a previous paper, increasing the mystery.

Then, it occurred to me that the Jurgens model is designed to explain normal speech CONTROL, not the loss of control that occurs in stuttering. In other words, using it to guide stuttering research areas — particularly for brain scan research — is nonsensical: a classic case of thinking within the box.

I’ll talk about what elements of the model are on the margins of the box next. They are very interesting.

Is Stuttering an Emotion?

There has been a lot of talk lately about the effect of emotions on stuttering and stuttering development.  Something that hasn’t been considered, however, is the possibility that stuttering itself is a response to an “emotionally competent stimulus,” which would mean that stuttering qualifies in some sense as an emotion.

An “emotionally competent stimulus” is an object or stimulus that is real or directly recalled from memory. In the case of disgust, for example, an ECS could be an actual pizza covered with maple syrup or a memory of one. In the case of stuttering, an ECS could be an actual situation, such as speaking to a particular person (say, an authority figure) who is associated with a severe stuttering event.

The more interesting possibility, however, is that an internal feeling of loss of speech control (which could be quite subtle) could be an ECS. What’s interesting about this possibility is that it could bridge the gap that is present in all mechanical theories of stuttering between a relatively subtle internal impairment (e.g., the now well-documented white matter anisotrophy in a major speech-language/ motor neuron circuit) and the resulting speech impairment, which can become severe in a matter of hours or days in young children.

The real interest here is that as the ECS develops, so would the intensity of the emotional (i.e., stuttering) response.

Effect of False Body Maps on Stuttering Development

Loss of awareness of stuttering events is a well-known phenomenon to which any stutterer who has viewed a video recording of his own speech can attest. An extreme manifestation is “le petite mort,” a name given by Van Riper to the actual loss of consciousness that can occur in severe stuttering.  (I remember my own horror at viewing a video of my eyes rolling back into my head during severe blocks I could not remember.) What apparently happens here is that the periaqueductal gray (PAG) in the brain stem, triggered by the amygdala, sends messages to nerve pathways that would normally convey signals of painful or aversive sensory inputs, that block awareness of the input. This is a highly adaptive trait, in that the person can continue basic life functions in the presence of emotional or physical damage, potentially fleeing or controlling a highly dangerous situation. It explains why people in catastrophic accidents do not initially feel pain; and why stutterers can continue to speak when they are experiencing chaotic speech events that would probably cause a fluent speaker to stop dead in his/her tracks.

Given the similar neurological reactions to emotional and physical pain, it is interesting to explore the possible implications of the filtering out of  body signals during emotionally painful stuttering events.  Such an events might include, for example, a particularly violent tremor, a twisted tongue pushed forward out of the mouth, jaws locked in a hyper-extended open position, or any other movement caused by a reaction to loss of speech control.  Note that, while these are events commonly labeled as “escape behaviors,” they are the result of virtually automatic reactions that occur below the level of immediate awareness.

I’m keying off  a discussion that can be found on page 111 ff in Antonio Damasio’s 2003 book, Looking for Spinoza, in which he notes that “the brain effectively eliminates from the central body maps [involved in the creation of feeling states] the patterns of activity that would permit the experience of pain.” (It has been known for some time that physical pain and aversive events that cause emotional pain are handled in similar ways by the brain.)

To understand why such a system would be present in humans, we only need to consider the importance of speech in human survival.  But that’s another subject, and a very complex one at that.

To continue to the point, lack of awareness of the various tensions, tremors and maladaptive movements and postures involved in the loss of speech control associated with stuttering would quite possibly result in the creation of a “false body map” — a sort of hallucination of normalcy that would: 1) deprive the stutterer of  feedback required to determine if the speech system was ready and optimised for fluent speech, 2) enable the stutterer to persist in the attempt to speak in the presence of a disabled speech system; resulting, however, in continued stuttering.

Given our knowledge of the pervasive role of conditioning in human behavior, such a circumstance could not be positive for the maintenance of fluent speech. Particularly when it would enable the massed repetition of negative conditioniing events.

I happened to be reading a stuttering listserv awhile ago and noted one correspondent bitterly complaining that he was blissfully unaware of his childhood stuttering until he received speech therapy.

However, given the concept of “false body maps,” could interrupting this blissful state be yet another argument for the value of early intervention?

Feeling the Loss of Speech Control

Greg has a really interesting concept on Stuttering.Me: the notion that  “stuttered speech is nothing more than a reflexive behavior that the body uses to deal with the stuttering phenomenon (which is best represented as a neurological state).”  If the neurological state includes the disconnection of speech control (and sometimes the awareness of this loss of control through feedback from the body), then this notion makes a lot of sense to me, as does his idea that “we produce stuttering behaviors to kick-start (or get out of) our stuttered neural state.” Looked at in a slightly different way, this is basically saying that going ahead and speaking, in spite of the feeling that we are blocked (which may result in overt stuttering behavior) is a way of  resolving the block.  He concludes this by saying that “stuttering has 2 components; the stuttered neural state, and a reflexive behavioral compensation to the stuttered neural state.”

We are then left with the question: where does the “stuttered neural state” come from?

That’s the question we’re exploring here.  The key may be that we can sometimes actually feel that the loss of speech control is present. This feeling is the result of our awareness of underlying reactions and emotions (neurological phenomena and the resulting body state.)  Resolving this feeling and state is the theory behind preparatory sets.