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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: “yup, 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.
Why would the hippocampus (of all things) be involved in speech?
I’ll discuss that next.
(Revised 7/1/2010)
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.
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.
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?
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.
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.
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.
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.
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.
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.
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