Upcoming Events

There are no upcoming events.

Why Real Research in Stuttering Brain States is Needed

Until real research that considers the role of emotions and conditioning in stuttering is performed by credible researchers, these key elements of stuttering will remain in the hands of “cognitive therapists” who promise that they can help stutterers “think their way out” of stuttering by changing the semantic evalutions of feelings that people have when they stutter.  To the contrary, recent research (not associated with stuttering, unfortunately) is finding that emotions are largely formed by subconscious reactions to internal and external stimuli and that there is a progression from emotions of various types to feelings. Emotions are behaviors, which places them in the realm of stuttering behaviors, while feelings are thoughts about emotions (what Antonio Damasio calls “brain maps”), which places them in the realm of thoughts about or semantic evaluations of stuttering. While there is some ability to cognitively influence evaluations of emotional states, semantic therapies are dealing only with top-level thought processes and can only indirectly influence the underlying reactions and responses that trigger the emotions that accompany stuttering behaviors.

Further, many of the primary stuttering emotions supposedly targeted for extinction by semantic or cognitive approaches are completely rational (if unhelpful) in the context of stuttering. For example, I read an endorsement of neuro-semantics by one SLP (who should know better) expressing amazement that people could actually fear stuttering. To change or extinguish these emotions, one first needs to change the underlying reactions that are creating them.  That would seem to require work to modify actual stuttering behaviors in some way, shape or form.

Reactions before emotions; emotion-caused behaviors before feelings; feelings before thoughts about (or evaluations of) feelings. You can only partially reverse-engineer this progression. Semantics or linquistic arguments may work for people with cognitive and emotional disorders, but stuttering involves actual neurological characteristics and probable neural modifications over time  that language alone can’t begin to compensate for or extinguish.

Stuttering Brain State

Reading Antonio Damasio’s “Looking for Spinoza: Joy, Sorrow, and the Feeling Brain,” and was struck by the description of a “Decision-Making Mechanism” that starts on page 144 — thinking how it could relate to stuttering behavior. Damasio believes that his research supports the idea that emotions in people with properly functioning brains are inherently rational, in that they are a direct response to stimuli that are “emotionally competent,” (i.e., capable of stimulating an emotion.)  Therefore, he believes, these emotions are an important aid to rational decision-making. His focus is primarily on the effect of brain damage resulting from trauma or stroke, but he also brings up the situation of people whose “life maps” are “systematically false” for one reason or another (he uses brain changes due to addiction as an example.)

Now, it occurred to me that there is something to say about behavior disorders in all of this; particularly a behavior like stuttering that involves a number of strong emotions that are linked in a special way to partly (or in some cases, mostly) unconscious (and possibly automatic) decisions like: the amount of tension used to produce a particular sound, which word to say and which to avoid, whether or not to speak in a given situation, whether or not to use a particular speech modification technique, or even whether to go to school on a particular day.  Note that some of these involve speech and others involve speech- or life-participation activities.

If stuttering is interpreted by the stutterer (consciously or unconsciously) as an inherently dangerous behavior (as it certainly can be in some situations we find ourselves in), there would be many situations when this evaluation and the resulting decisions would clash with some competing needs, such as the need to go ahead and speak during a job interview, oral academic exam, or meeting an interesting member of the opposite sex.  But enough of this speculation for now.

My point in raising Damasio’s research and hypotheses is this: where in the field of stuttering is there anyone doing anything to study the dynamics of emotion in stuttering in anything like the richness and complexity that Damasio discusses?  Researchers seem to be stuck on anxiety as the primary emotion involved with stuttering, when in fact there are many many more emotions involved in the complex brain state that accompanies stuttering, (and in particular, severe stuttering), including:  shame, embarassment, fear, anger, panic, impatience, struggle, confusion, hope, despair, etc. etc. All of these form a rich stew of emotions that the stutterer must process (or attempt to ignore through temporary loss of awareness) as he or she is trying to form some thoughts into coherent statements that can be understood by listeners. Each of these emotions has its own brain signature. The resulting feeling state is probably unique to the individual, but perhaps similar in some respects across the stuttering populations. 

Wouldn’t it be more fruitful to investigate this brain state, which is occurring at the time the stutterer is speaking, than to fixate on anxiety, which is an emotion /brain state that is anticipatory with respect to stuttering and which is quite possibly overwhelmed once the stutterer begins to speak?

We now have a lot of data that could be used, but they continue to be interpreted only as the signature of mechanical brain operations involved in producing speech. And the data have possibly been processed in a way that reflects the biases of the researchers who collected it. One example of this would be the theory that anomalous right hemisphere activity in stutterers indicates the use of that hemisphere to plan speech motor movements,  rather than seriously looking at the possibility that a lot of emotional processing is occurring there as well.

Promising Research Takes “The Path Most Traveled?”

Two significant research studies  (paper 1; paper 2) by a Chinese team led by C. Lu have provided additional evidence that weaknesses or characteristics in the connectivity of circuits between brain activity centers involved in speech-motor movements is a key to understanding stuttering.  However, as in previous work by Sommers (2002), there is no consideration given to an actual mechanism that would cause these characteristics to result in stuttering  in some situations but not others … and would explain the recovery of a significant degree of fluency following therapy.

I haven’t read the complete text of these papers yet, so I can’t speak definitively about them, but the concluding lines of one of the abstracts reveals some distressingly conventional thinking: “These results indicate that the large-scale dysfunctional neural interactions may be involved in stuttering speakers’ difficulties in planning, execution, and self-monitoring of speech motor sequence during word production.”

Notice the lack of an actual consideration of the behavioral dynamics there.  It is almost tautological that researchers will find physical brain correlates of “planning, execution, and self-monitoring” problems in stutterers.  However, very few of these research studies look at the actual dynamics of the behavior and develop some useful or even interesting hypotheses about the mechanism.

So: why does stuttering happen sometimes and not others? Isn’t that the actual thing that could be modified in all this?  Isn’t that what researchers should be focusing on?

I think the problem is that many (most? all?) of the people performing research on stuttering simply lack the creativity and imagination to develop a useful hypothesis that would consider the full range of our understanding about the brain’s motor, emotional, and feeling mechanisms in the context of a social disorder.

I’m anxious to find out that I’m wrong about these papers, so I’ll be trying to get my hands on them.

Space Vs. Time in Stuttering Therapy

One way of looking at overt stuttering behaviors is to see them as resulting from a reaction or defense against the unpleasant feeling of the speech void — the feeling that we know what we want to say, but can’t for the moment figure out how to make the sound. This is the actual speech block, and it occurs in the brain, though we are made aware of it by the mind.

In the worst cases, we feel and react to the block, go ahead and try to speak in spite of it (using an increasingly more complex array of unsuccessful strategies), and fall prey to the chaotic series of movements, escape attempts, blackouts, and emotions that characterizes our particular brand of stuttering.

One rationale for the clinical use of delayed auditory feedback (DAF) in stuttering therapy is that it replaces a focus on the auditory feedback of speech with kinesthetic and proprioceptive feedback, or the “feeling” of speech.  I’m referring here to using DAF to generate very deliberate, “high stimulus” speech, featuring exaggerated articulation, mouth opening, and deliberate, relaxed breathing — not the rapid, quasi-fluent speech that such devices allow for those seeking quick fluency.

The concept behind this is to increase the stutterer’s ability to feel his/her way through episodes of disfluency by shifting from the (theoretical) “internal” speech loop to the (theoretical) “external” speech system when experiencing a stuttering block. This enables the use of techniques such as cancellations, pullouts, and preparatory sets. Some therapists (like Walt Manning) even view the capability to make this transition as a central part of the change process for people who stutter.

Another way to look at this is that the more “automatic” internal loop is dominated by auditory feedback and the time domain, while the more “deliberate” external loop is more closely associated with kinesthetic and proprioceptive feedback and the space domain. Of course, this is more a matter of emphasis, as the systems actually seem to work together.

When viewed in this way, a lot of things about stuttering therapy seem to make more sense, in particular the connection with emotions and feeling that differentiates stuttering therapy from other kinds of speech treatment.

It also leads the way to thinking about supplemental alternative therapy approaches that can be helpful; in particular, those that are descended from Eastern (space-oriented) philosophies rather than Western ones — most of which are tied closely to the time domain. It’s not a coincidence that the Eastern approaches focus on dissolving conditioning and the ego, while the Western ones attempt to build the ego to deal with stress, time pressure, and all of the other ills that face people in developed countries.

More on this later.

Lessons from Haloperidol

Back in the 1970’s there was a miracle drug on the horizon that promised relief from stuttering. Haloperidol (also marketed under the name Haldol) was touted as “work[ing] specifically to counteract a source of motor timing irregularity in stutterers” (Prins, Mendelkorn, Cerf 1980.)

With stutterers now pouring their hopes into the promise of a Pagoclone Phase III trial, it might be worthwhile to reconsider the history of Haloperidol. 

Like Haloperidol, Pagoclone is touted to ease the “coordination breakdowns”  that neurologists like to provide as evidence of neurotransmitter (the D2 form of dopamine) and other motor speech explanations for stuttering. This in spite of the fact that Pagoclone (unlike Haloperidol, Risperidol, etc.) is basically a partial GABA agonist that increases the action of some inhibitory GABA neurons that are located in many brain areas, but are especially dense in several amygdalae nuclei.

The complex “gate-keeper” role of GABA in disinhibiting feed-forward, dopamine neurons projecting from the amygdala that normally reduce inhibition is discussed here: doi:10.1016/j.neuron.2005.12.002  But the role of the amygdala in the action of Pagoclone does not seem to be mentioned anywhere in the literature.  In addition, although GABA neurons are housed in the basal ganglia (the prime structure involved in voluntary motor actions) it is not entirely clear how the  GABA neurons’  inhibition of dopamine neurons is going to be restricted to the basal ganglia to prove the pure motor theory of stuttering (I’m being facetious here), or if they will even be particularly active there in quite the manner anticipated. An imbalance of D1 and D2 neurons (the theoretical “problem” underlying much of this) has primarily been noted in children … and children are not even going to be involved in the Phase III trial.

In short, there is no experimental explanation appropriate to Pagoclone of how this rebalancing act is going to work.

Now, back to Haloperidol. In the research by Prins, et. al. cited above, no motor action effects were found.  Instead, the authors found that “[a] more reasonable interpretation is that it was effective for most subjects in producing a general reduction in vigilance” (bold italics added.) This would be more consistent with an inhibition of reactive conditioning (an amygdala activity.)

So, how do these drugs work? No one really knows, and Pagoclone has flunked its previous trials as an anxiety medication. In the Phase II trial for stuttering, Pagoclone is widely known to have been effective for 55% of the treated patients, while the placebo was effective for 36% of the treated patients. And what “effective” means in this case hasn’t really been defined. I’m wondering what the excitement is all about.

Fear Memory Erasure Redux

Now that I’ve had a chance to read the entire research article in Science (search “Han Selective Fear Erasure” in PubMed) I’m more convinced than ever that this research could — if a host of human application and potential subject safety issues are addressed — have application to detecting lateral amygdala (LA) activity associated with fear conditioning while a test subject was stuttering.

To date, PET and fMRI brain scans have been unable to detect such activity in stuttering subjects because they are simply too crude to image routine activity (such as chronic stuttering) in the LA, which may involve only small numbers of neurons triggering distributed response circuits. Researchers who study stuttering commonly confuse such activity with the high activity that would occur during response/reaction to an extremely threatening novel stimuli. (This is possibily indicated by the fact that broader amnesia was produced when researchers used their technique during training of novel stimuli.)  

The research involved selective erasure of a specific fear memory that associated an auditory tone with an electric shock by use of a clever technique that allowed ablation of only those neurons that were involved in the expression of that memory. Other memories and ability to create new fear memories (critical to human survival) remained intact. The methods and controls employed in the research seem to be rigorous, but then, this is a specialized area of experimental biological research.

Enabling the Iceberg?

A new stuttering-specific spin has been proposed in the increasingly tiresome controversy about the use of “person first language” versus “calling a spade a spade:” the notion that using the moniker “person who stutters” instead of “stutterer” may “enable the [stuttering] iceberg.”

While most readers are probably familiar with the person first language (or PFL) controversy, the Iceberg may not have as much currency. The “iceberg of stuttering” was an analogy (actually more of a metaphor) first proposed by media-darling Joseph Sheehan to help people understand the insight that the visible part of stuttering (the observable speech behavior) was actually only a very small part of the human behaviors, attitudes, beliefs, experience, memories, and neurological characteristics that were associated with stuttering. It has recently been transformed (I think unhelpfully) into a full-blown analogy

I personally think the iceberg analogy is unhelpful because it’s an attempt to map out an area of the human mind as monolithically devoted to stuttering behavior — which could be falsely interpreted by some as comprising the totality of the mind, psyche or identity. It also offers the possibility of creating a rather cumbersome self-image, one that is based on a projection of the human psyche onto objective reality (and visa versa, sort of like Moby Dick.)

The idea that using the term “person who stutters” will actually “enable” the psychological and neurological underpinnings of stuttering originates in the notion that “denial” of stuttering is an unavoidable consequence of buying into an attempt by some (well-meaning) people to emphasize the “humanity” of the stutterer.  Stutter.Me (most of whose work I enjoy) uses a YouTube clip of “Malcom X” [sic] refusing to provide the Anglicanized surname of his father to make the point that stutterers should reject names provided by others. What Malcolm was denying was not his father’s name, but the “acceptable” self-image for a black person with which the interviewer was attempting to label him.

As for “enabling” the iceberg, it would seem that the real correlate of the pop psychology embodied by the analogy is not really something that can be enabled, but something that just comes with the territory. But it would seem to me that any behavior transformed into a thing (reified) and cast as someone’s identity would just be creating another unhelpful self-image.

I am my conscious awareness. If my consciousness of myself is mostly comprised of a list of self images, such as “runner,” “astronomer,” “avoider,” or “stutterer,” that’s a rather limiting pile of illusions for me to have: the working through of which is part of the task involved in development. If I buy into the idea that I have a monolithic, reified pile of garbage or “thought stuff” in my mind associated with each of these roles, rather than (as I think) some distorted self-images associated with behaviors and feeling states that invite inquiry, how am I going to proceed? And what difference does it make if the term I use to describe myself is “person who stutters” or “stutterer?” (I am perfectly comfortable with either one.)

My ultimate purpose as a social human being is to expand my conscious awareness and deal with the conditioning that hinders this process. The best way to do this is through awareness and exploration of behaviors, feeling states and physical deconditioning, not thinking experiments like icebergs or hexagons. When I realize that behaviors or descriptive terms have nothing to do with my true identity they cease to be who I think I am and become merely false self-images. When I obsess about what I call myself or what people call me, that’s an indication that I might be restricting my consciousness because of such self images. When I hear someone talk about “getting my hexagon in order” it makes me want to scream.

Reification of stuttering is actually one of the problems associated with the behavior that begin to be resolved if we can stop labeling stuttering as negative or positive and start seeing it as just … what is. This is difficult but necessary work. It will always be incomplete. But it will have to be started at some point.

LeDoux & the Amygdaloids

Came across this old blog from April 2008 showing Joseph LeDoux of NYU explaining some of the basic features of his research on the “emotional brain” and threat and fear conditioning, followed by a funky (and perhaps, to some ears, lame) rock song about wanting to take drugs to erase fear memories — something that is not going to happen, of course, as they are indelible.


Unfortunately, I think this attempt at popularization plays into the public’s misconceptions about fear conditioning. One can’t really “wander around in the mind” pointing out instances of such conditioning. These are particular types of memories that are inaccessible to the conscious mind, as LeDoux points out in the lecture segment.  We can access traumatic memories and some experiences where fear conditioning may have taken place. But we can’t mentally access the root conditioning and we certainly can’t get at the neural circuits that implement behavior modifications. The only known ways of influencing these circuits are drugs, deconditioning activities and behaviors (therapy), surgery (which at the moment is extremely crude and not worthy of consideration,) and possibly the kind of control claimed by some yogis. We can talk to our fear memories all we want, but we might as well be talking to a wall.

In addition, fear is actually a reaction to threat responses and requires a particular type of sensitivity to the physical changes caused by these responses or the later conditioning. We need conditioning to stutter (by exploiting vulnerabilities in the speech system), but we apparently don’t need fear (or a conscious reaction to our conditioning and the resultant behavior) to stutter. There are some stutterers who claim they don’t feel any fear at all when they stutter. I believe them. There is much stuttering of which the stutterer is simply unaware.

Awareness of Stuttering

The poet W. S. Merwin used an epigraph from Heraclitus in his fine early collection “The Lice” that has since reminded me of the value of becoming more and more impeccable (not “perfect”) about catching stutters and cancelling them:

“All men are deceived by the appearances of things, even Homer himself, who was the wisest man in Greece; for he was deceived by boys catching lice: they said to him, ‘What we have caught and what we have killed we have left behind, but what has escaped us we bring with us.'”

Fear Conditioning Erased in Mice

[Blogger note: The title of this post has been changed to more accurately reflect the subject of interest]

My friend John Paskievich sent me a link to a fascinating article in ScienceNOW.

The article describes a research study that demonstrated the selective erasure of fear memories in the lateral amygdala of mice, using a genetically engineered “switch” that allowed neurons that produce CREB (a protein implicated in fear memory formation) to be located and killed when they produced a response to a fear-inducing stimulus. Until now, it has been thought that such procedures would result in the erasure of all memories in a brain region. The targeting technique use in this case left other memories intact. The application for stuttering is obvious, assuming that scientists could learn how to target the more human CREB neurons in this manner while subjects were stuttering. Obviously, there’s a lot of ground to cover before that would be tried. Here’s the link: