Some keys to understanding stuttering and its management
by Professor William Webster, PhD
In this edited version of a presentation given to the SpeakEasy Symposium in May 1995, Professor William Webster (Dean, Faculty of Social Services, Brock University, St Catherine's, Ontario) spells out his theories about the causes of stammering. He pays special attention to the variability of stammering, the perennial question of "Why can't I say today what I could so easily say yesterday!".
I began my research into stuttering some years ago because of my experiences with stuttering variation and my curiosity about what might underline it. This variation in severity makes stuttering such an interesting phenomenon scientifically and phenomenologically.
Because of my scientific background the focus of my research has been on the brain, and two questions in particular have guided my research: 1. What is different about the brain of the person who stutters compared with the brain of the person who does not stutter? 2. What changes in our brains as we go from periods of fluency to periods of dysfluency?
We should bear in mind two general points about the brain as a biological organ. First the proposition that the brain is the organ of the mind and behaviour is well accepted. This proposition implies that if two people differ in their behaviour (stuttering vs non-stuttering), their brains are functioning differently. Similarly, it implies that when behaviour changes from one time to the next (fluent speech to stuttering), something has changed functionally in the brain. The research has been directed towards understanding the nature of these differences and changes.
The second point is that anatomically the brain is comprised of two halves or hemispheres that look more or less the same and are connected through a large bundle of nerve fibres called the corpus callosum. Within each hemisphere is a very large number of individual cells called neurons, and these interact with one another at junctions that are called synapses. The nature of the interaction is chemical, which means that anything that affects the chemistry of the brain and affects the interactions among neurons will affect the mind or behaviour at some level.
The overall point is that from a neurological perspective what ultimately differentiates the person who stutters from the person who does not stutter is related to i) neurons, ii) how those neurons are connected and iii) what occurs chemically at the synapse. Similarly, when stuttering severity change, it is due ultimately to changes at synapses. Unfortunately, we are far from the stage technologically or conceptionally where we can even speculate meaningfully about what is happening in individual neurons and at individual synapses that leads to stuttering. As will be evident, our models are still at a global or conceptual level.
Models of Stuttering
One of the earliest ideas about what is going on neurologically in the person who stutters comes from a model developed in the 1920's by the neurologist Samuel Orton and the Psychologist/Speech pathologist, Lee Travis. As illustrated in Figure 1A, they argued that, in contrast to the fluent speaker, the person who stutters has speech centres in both hemispheres, each of which issues commands to the peripheral speech apparatus. This leads to discoordination of the speech apparatus resulting in speech disruptions. Presumably, variation in stuttering severity would be related to the degree of asynchrony of commands.
When I began to address the questions of 1) what is different about the brain of the person who stutters and 2) what changes in the brain of the person who stutters corresponding to the changes in stuttering severity, this model was the starting point for my studies. The approach to studying brain mechanisms I have persistently taken is indirect. I study the organisation and co-ordination of movements by the hands of people who stutter, and infer something about the organization of speech motor control mechanisms. The approach is based on the assumption, for which there is good evidence, that the neural mechanisms of speech overlap those for the control of fine finger and hand movement. I believe we can learn about speech by studying the control of finger and hand movements, and by doing so we avoid all the problems of studying speech directly when speech for so many of us is anxiety provoking.
To test the Orton Travis model in our initial study, I looked for evidence that the mechanisms for fine motor control of the hands may be bilaterally represented in people who stutter. The prediction under the Orton Travis model is that, having bilateral mechanisms for speech and other forms of fine motor control, people who stutter should not show a right hand advantage in sequential finger tapping. Both hands should perform equally well (or poorly).
The results of our first study showed clearly that people who stutter perform sequential finger tapping in a manner virtually indistinguishable from fluent speakers. Our interpretation of this result, consistent with data using other approaches, is that people who stutter have a normal left hemisphere lateralization of speech and fine motor movement functions.
One concern we had about this particular finger tapping task is that it is quite unlike speech, in that the same movements are performed repetitively. In speech, however, we initiate new sequences of movements, and indeed one of the real problems for people who stutter is saying new things. Accordingly we devised a different finger tapping experiment that required the participant to reproduce sequences of finger movements that changed from trial to trial. We found that people who stutter proved to be slower to initiate the sequences. They also made more errors in tapping, but tapped as fast as fluent speakers once they got started. The implication of these data is that there is a general problem in the planning, organisation and initiation of movements, including speech. Although there is normal left hemisphere specialisation for speech and sequencing movements (as shown in experiment 1), the mechanisms clearly do not work as efficiently as they should. And the inefficiency relates in particular to planning and initiating movements.
In considering the question of variability, which is the key to understanding this phenomenon of stuttering, we developed and tested a model that we call the Interhemispheric Interference Model. As illustrated in Figure 1B, the model has three major features to it: i) normal left hemisphere lateralization; ii) normal right hemisphere functioning; but iii) interference with the left hemisphere coming from the right hemisphere through a "slop-over" of activity (the large arrow). Within this model, variations in stuttering severity would reflect variations in the amount of overflow from the right to left hemispheres.
To test this model, we exploited the fact that each hemisphere controls the opposite hand and the natural tendency for two hands to work together in a mirror-image manner: so excessive overflow should make it difficult for people who stutter to co-ordinate different hand movements by the two hands. In two experiments we had participants perform the sequential finger tapping and sequential reproduction tasks described above while carrying out another activity (turning a knob back and forth whenever a tone sounded) concurrently with the other hand. In a third experiment we asked participants to write letters simultaneously with the two hands. In all experiments we were interested in the interference under the concurrent task conditions. Not unexpectedly, all subjects showed poorer performance on the finger tapping and writing tasks with the right hand when performing the concurrent task with the left, but the important finding was that this task interference was greater among the participants who stuttered. The results were consistent with the model, and we took this as evidence of overflow.
While I continue to believe that interhemispheric interference is a factor, and an important one, our more recent research had indicated that the critical mechanism for that interference in fact is not ungated or unregulated overflow of information. The studies indicate instead that there are two brain anomalies involved. These are illustrated in Figure 1C in what we call the Two-Factor Interference Model. Three elements comprise this model: i) we still assume normal left hemisphere specialisation for speech and motor sequencing; ii) we see a left hemisphere system for speech and motor sequencing that is inefficient and unusually susceptible to interference (illustrated by the larger number of "pores"), not just from activity in the right hemisphere, but also the left (illustrated with arrows from both hemispheres impinging on the speech mechanisms); and iii) a lack of what we call "left hemisphere activation bias" (illustrated with equal rather than unequal sized arrows coming from the mid-and hind-brain activating system).
We believe that the area that is fragile and susceptible to interference is what is called the Supplementary Motor Area. Located on the upper medial walls of the hemispheres, it is particularly important for the planning of sequences of movements, including speech. Especially relevant for the model, the supplementary motor area of the left hemisphere has very close connections to the right hemisphere through the corpus callosum, leaving this area ideally positioned for interference by activity of the right hemisphere.
We also believe that right hemisphere overactivation is important in the process. Recent research suggests that normally the left hemisphere is in a state of greater readiness or activation than the right. We have data now which suggest that in people who stutter the two hemispheres are in a state of more equal activation, even greater activation in the right than left hemisphere. The significance of this finding comes from the critical role played by the right hemisphere in the mediation of emotion. We know from research that when we experience positive emotions that motivate us to approach a situation, the frontal portion of the left hemisphere becomes increasingly active. In contrast, when we experience negative emotions like fear and anxiety and apprehensive emotions that motivate us to withdraw from a situation, the frontal portion of the right hemisphere becomes increasingly active.
What this all then leads to is the suggestion that the fear and apprehension associated with stuttering affects speech by being associated with right hemisphere activation, activation that interferes with the left hemisphere supplementary motor area which results in turn in greater stuttering. This stuttering then reinforces the fear and apprehension of being in the speech situation. There is, therefore, an important interplay between the neurology and psychology of stuttering that is shown schematically in Figure 2. The origin of stuttering is to be found in anomalous brain mechanisms, but the fear and apprehension that become part of the phenomenon of stuttering contribute to the stuttering by acting on the anomalous brain mechanisms as illustrated in the figure.
What does this model tell us about the management of stuttering?
The first point I would make is that the research indicating anomalous brain function associated with stuttering is consistent with the ever increasing body of literature suggesting a biological basis to stuttering. Our own work has suggested that about two-thirds of adults who stutter report a family history of stuttering. But families share not just genes but also experiences, and so more compelling evidence comes from the study of identical and fraternal twins. Identical twins have of course, the same genetic make-up while fraternal twins are genetically no more similar than other siblings. Research has estimated the risk of stuttering in the identical twin of a person who stutters to be 0.73 while that in the fraternal twin of the person who stutters is only 0.32. If there was no genetic component, the risks would be identical.
This kind of evidence suggests two things: 1. First, the cause of stuttering is to be found in our biology, and in most cases (but not all) the critical elements of biology are influenced by our genetics. The cause is not to be found in what Mom or Dad did or did not do to us. However, the research I described earlier would also suggest that what Mom and Dad did or did not do, or what our experiences have been, will very much affect the severity of our stuttering if we are predisposed to stuttering. Our apprehension, fears, anxieties and expectations about stuttering will affect the severity of our stuttering through the mechanism of interhemispheric interference.
In other words, our experiences affect our emotions: our emotions affect our brain (in particular the right hemisphere in the case of negative emotions): and activity in our right hemisphere in turn affects what is happening to the left hemisphere.
2. The second point I would leave you with follows from the first and relates to the management of stuttering within ourselves.
It has become clear that cure or reversal of stuttering is unlikely. The management of stuttering involves establishing control over the brain. Our current model suggests that successful therapy (or management) has two components:
a. Removing sources of interference with speech by reducing right hemisphere activation. We need to overcome avoidance, withdrawal, and apprehension. When we do this, we reduce the tendency to withdraw from the feared situation, and the right hemisphere activation associated with these emotions decreases. This is turn means less interference with the left hemisphere Supplementary Motor Area.
b. Secondly, we need to counteract the fragility and inefficiency of the left hemisphere system. By making controlled and deliberate speech motor movements, slowing and simplifying our speech, we may focus activity on that system and bring speech within the capability of the system.
3. Thirdly, although there is a biological basis to stuttering, although there is something different about the brains of people who stutter, it does not mean that stuttering is inevitable. Biological does not mean inevitable, even when biological is the brain.
However, it is now clear that not only is the brain the origin of behaviour, but behaviour is the origin of brain function. Not only does consciousness emerge from brain function, but consciousness affects brain function. Not only does thinking result from brain activity, but thinking itself affects brain activity. Not only do our emotions emerge from the activity of the brain, but our emotions drive the activity of the brain. Consequently, when we voluntarily control our speech movements through monitoring, regulating speed, controlling breathing and voice onset, and being deliberate in our speech, we are in effect controlling left hemisphere activity. Similarly, when we voluntarily control our fears and anxieties and apprehensions by using techniques like progressive relaxation and positive self-talk, and when we systematically go into feared situations so we become less fearful, we are doing things that will affect our right hemisphere. And when we control the right hemisphere, we minimise interference with the left and we minimise stuttering.
In other words, when we use techniques to control our speech and to control our emotions, we are using techniques to control our brains. Although our brains may have a certain propensity to operate in a certain way that results in stuttering, I would suggest that, within limits, we can overcome that propensity through voluntary control.
From the Autumn 1996 edition of 'Speaking Out'.
© Professor W. Webster.
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