A Theory of Stuttering

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Introduction

There are many theories of how developmental stuttering may be caused. By now, some of them have definitely been filed away; for instance, stuttering as a neurosis, as a muscular spasm, or as a learned behavior. Today, experts agree that stuttering has to do with a malfunction in the brain. This is suggested by a lot of empirical data; however, we don’t know how the deviations in brain structure and function that were found make people stutter – that is, how they make them, against their will, repeat words or parts of words, prolong speech sounds, or get totally stuck.

Stuttering cannot be explained by simply saying that speech control breaks down, although a person whose speech is suddenly blocked may subjectively experience this as a loss of control. A breakdown of speech control could manifest in completely other symptoms as well. Why doesn’t an incomprehensible babbling or mumbling occur? Why does the person not yell or talks nonsense – or what else one may imagine as speaking out of control? Why do just those specific symptoms occur – those that we refer to as stuttering? What causes them? What is the underlying mechanism? Solving this problem should enable us to answer many other questions related to stuttering, such as:

How do the core symptoms (repetition, prolongation, and silent block) come about? If something goes wrong in the brain, why does it manifest in three different types of symptoms, and why just in these?

Why does stuttering mostly and at the earliest onset when children start forming sentences, whereas previously, during the babbling phase and the period of one- and two-word utterances, the same children didn’t show any symptoms?

Why do most of the affected children spontaneously recover from stuttering after some months or years, and why do many more girls than boys recover?

Why is stuttering so influenced by situations, by the environment, or by the number and the kind of listeners? If something goes wrong in the stutterer’s brain, why does it affect speech in some situations, but not in others?

What relationship exists between stuttering and linguistic structure? Why is one sort of initial sounds (stop consonants, vowels...) more frequently stuttered by one person, another sort by another person? Why does stuttering occur mostly at the onset of words and always at the initial part of syllables? Why are stressed syllables, long words, and words with high information load more frequently stuttered?

What role do the structural and functional abnormalities play that were found in the brain in stutterers? Which of them is causal for the onset of stuttering, and which is causal for persistence? Which ares merely concomitants or consequences of the disorder?

Why can certain conditions, such as choral speech, paced speech, altered auditory feedback, or auditory masking by loud noise, dramatically reduce or even eliminate stuttering?

Why is stuttering, at least in some cases, successfully treatable by an alteration in behavior, for instance, by applying a special speech technique? If something goes wrong in the stutterer’s brain and causes the disorder, how can a behavioral change repair this or compensate for it?

Finally, the most important question a theory should answer is: Can persistent developmental stuttering be cured, and if so, how? And if not, what can be done to alleviate the symptoms? In other words, what is the best therapy? ?

The present theory will be able to answer these questions. Two things are assumed to play a central role in stuttering: the processing of auditory feedback and the regulation of attention during speech. For a long time, auditory feedback – hearing onself speak – has been suspected to be involved in the mechanism underlying stuttering. Stuttering is often significantly reduced or even disappears as long as one’s own speech is perceived in an altered and unfamiliar manner, either by an alteration of speaking or by an artificial alteration of the auditory feedback. This is, for instance, the case in chorus reading, shadowing, in speaking in an assumed voice or in an unfamiliar dialect, but also with auditory masking (by loud noise through headphones) or with artificially delayed or frequency-altered auditory feedback (see Bloodstein and Bernstein Ratner (2008) for an overview).

Most researchers believed that hearing oneself speak caused or exacerbated the disorder (e.g., Sandow, 1889; Cherry & Sayers, 1956; Maraist & Hutton, 1957; Yates, 1963; ; Van Riper, 1973; Max et al., 2004). Consequently, they assumed that stuttering disappears or is reduced because, in the above-mentioned conditions, the stutterer’s attention is distracted from hearing his or her speech, such that auditory feedback is no longer or to a lesser extentinvolved in speech control.

However, brain imaging studies have shown that speaking in an altered manner or with altered auditory feedback is not associated with smaller but greater activations in the secondary auditory areas (superior and middle temporal gyrus, BA21/22) that are responsible for the processing of auditory feedback, among others. This contradicts the distraction hypothesis.

For instance, greater activations in secondary auditory areas were observed in stutterers during metronome-paced speech, chorus reading, and singing as compared with stuttered speech (see the table below). Greater activations in the secondary auditory areas were also observed in speaking with altered auditory feedback with normal speakers. Two meta-analysis of brain-imaging studies that examined the effect of fluency-enhancing conditions (Brown et al., 2005; Budde, Barron, & Fox, 2014) revealed that the lack of activation in the secondary auditory areas is one of the very characteristics of the brain activation in stutterers. (read more).

These results don’t support the hypothesis that distraction from auditory feedback improves speech fluency, not least because brain imaging studies with normally fluent speakers have shown that attentive listening to speech stimuli is associated with greater activation, but distraction from the stimuli is associated with smaller activation in secondary auditory areas (Jäncke, Mirzazade, & Shah, 1999; Hugdahl et al., 2003; Sabri et al., 2008).

A correlation between reduced stuttering and greater activity in secondary auditory areas was not only found with fluency-enhancing conditions. As listed in the table below, normal fluent speakers as well as recovered stutterers showed greater activation in these cortical areas during speech than persistent stutterers did. In some studies, a negative correlation was found between stuttering severity and activation in secondary auditory areas; that is, the severer the stuttering, the smaller on average was the activity in secondary auditory areas, and vice versa.

Furthermore, after a successful fluency-shaping therapy, participants showed greater activations in secondary auditory areas than they did before the therapy. The latter finding may appear surprising because fluency-shaping therapies don’t intend to influence auditory processing. However, participants may have monitored the correct application of the speech technique (gentle voice onset) by listening to their voice.

Table 1: Brain activation in the secondary auditory areas (in which the auditory feedback of speech, among others, is processed). In the seven lower rows, studies of fluency-enhancing conditions are listed. * = Meta-analysis

All the findings mentioned above suggest a relationship between auditory feedback and stuttering, but the nature of that relationship has hardly been understood until now. One reason is that the observations in this regard appear conflicting. On the one hand, stuttering disappears when auditory feedback is masked, delayed, or otherwise altered; this seems to suggest an effect of distraction. On the other hand, enhanced speech fluency is associated with greater activations in secondary auditory areas, suggesting a more intensive processing of auditory feedback. In the theory presented on this website, I will resolve this inconsistency and explain the relationship between stuttering and auditory feedback – a relationship that plays a central role in the mechanism underlying stuttering.

There is growing evidence of deficient attention regulation in. They seem to be less able to allocate attentional resources under dual task conditions, and they are more prone to exhibit attention disorders (see, e.g., Alm, 2014; Eggers & Jansson-Verkasalo, 2017; Ntourou, Anderson, & Wagovich, 2018; Wagovich, Anderson, & Hill, 2020). Other studies found deficits in auditory processing, among them in mechanisms underlying the automatic control of auditory attention (see a list of studies). As far as I know, these relatively new insights have hardly been included in a causal theory of stuttering until now. In the theory that I will propose here, attention control plays a central role, which allows us both to describe a brain mechanism that causes stuttering and to explain the influence of psychological, linguistic, and environmental factors.

The subject of the theory is developmental stuttering, not neurogenic stuttering caused by stroke, brain injury, or medication. I don’t use the term ‘psychogenic stuttering’, but there may be cases of late-onset stuttering in which it is hard to say whether they were caused more by a genetic predisposition or more by psychological or environmental factors, for instance, a trauma. A causal theory of developmental stuttering should include cases of late-onset stuttering, since the symptoms and the abnormalities in the brain are similar (Chang et al., 2010).

The position I start from is that developmental stuttering is a disorder of normal speech; that is, stutterers speak normally as long as they are spontaneously fluent, and when they stutter, then their normal fluent speech is disrupted. One may object that brain activation patterns in stutterers differ from those of normally fluent speakers and even during silent reading or thinking (see, e.g., Neumann et al., 2003). Do such findings not imply that stutterers never speak normally, not even when they are fluent?

To decide thi, we should distinguish between speaking, on the one hand, and the brain processes underlying speech production, on the other hand. For simplicity, let’s say that ‘normal speech’ is to string words together fluently with correct syntax and grammar. According to this definition, a stutterer who is doing so speaks normally, regardless of whether his brain possibly expends more effort or engages other brain regions, compared with a nonstutterer’s brain.

Maybe, stutterers’ brains are less suited for speech control; possibly, their structure is less optimal for this task. They may need a greater extent or a deviant pattern of activity for the control of normal speech. And i think we get a problem if we link ‘normal speech’ to a particular pattern of brain activity, as the brain activity during speech in different nonstutterers may differ as well. Therefore, I start from the position that stutterers speak normally as long as their speech is spontaneously fluent and sounds natural.

To understand stuttering as a disruption of normal speech, we first need to understand how normal speech production works and what role auditory feedback plays in it. That’s the topic of the first chapter.

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Footnotes

Stutterer

It may be considered politically incorrect, but I prefer using the good old term ‘stutterer’. I’m a stutterer, someone with a predisposition for stuttering who has developed persistent stuttering in childhood. Stuttering symptoms may occur when I’m speaking. From this, it doesn’t follow that I stutter at any certain moment. At the best, for example, after a successful therapy, a stutterer no longer or very rarely stutters, but nevertheless, he or she remains a (recovered) stutterer. The predisposition remains, and there is some risk of relapse. By contrast, the term ‘person who stutters’ (PWS), in my view, refers to someone who actually stutters. To be a recovered stutterer is possible, but a recovered PWS – a person who stutters who doesn’t stutter – isn’t it nonsense?

To call someone a stutterer, in my view, is more to attribute a property to him or her than to attribute a behavior. But it neither reduces the person to this one property, nor does it imply assumptions about personality traits, such as intelligence, competence, or self-assurance. Furthermore, abbreviations like PWS, PWNS, CWS, and CWNS don’t contribute to the readability and comprehensibility of the text; therefore, I avoid them. (return)
 

Shadowing

Speech shadowing is a technique in the treatment of stuttering. The stutterer immediately copies what another person, the leader speaker, e.g., a therapist, says, having only a vague or no idea of the words to be spoken until hearing them. The shadower has to listen to the leader speaker and is speaking at the same time, but not in unison with the leader. In this condition, stuttering usually does not occur (see, e.g., Cherry & Sayers,1956; Marland, 1957; Kondas, 1967). (return)

Quotations

Brown et al. (2005) wrote:
“Looking at the group comparison in the meta analysis, the area that showed the largest inter-group differences [i.e., between stutterers and controls, A/N] is a part of the superior temporal sulcus situated just anterior to those areas found to have voice-selective auditory representations […]. In sum, the published literature supports a robust auditory inhibitory effect in stutterers, which is consistent with the meta-analysis results.” (Brown et al., 2005, p. 113).

Budde, Barron, and Fox (2014) wrote:
“...left auditory (superior temporal gyrus) activations were greater in controls than in PDS, but bilateral auditory cortex activations were greater during fluency than dysfluency, especially on the right. No auditory cortex activations were present during dysfluency. Absence of left auditory cortex activation (compared to controls) indicated stuttering trait, and absence of right auditory cortex activation indicated dysfluent state” (Budde, Barron, & Fox, 2014, p. 104) – A/N: The latter may result from the fact that stuttered speech and induced, i.e., not spontaneous fluency were compared in the within-group analysis. Induced fluency is associated with greater activation mainly in the right auditory cortex. The reason may be that, in most fluency-enhancing tasks, stutterers only read, but not produce self-formulated speech; thus the left-hemispheric language network may not fully be activated. I think that self-formulated fluent speech requires auditory activation in the language-dominant hemisphere. (return)
 

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