A Theory of Stuttering
A Theory of Stuttering
“One of the riddles of developmental stuttering is its onset. No other developmental communication disorder presents such a profile of ostensibly normal development, followed by a transition into a pattern of disordered production. […] most children who stutter apparently display an early profile of normal fluent expressive communication, only to develop typically between the ages of 30 to 36 months, the disfluencies characteristic of stuttering […] What possibly changes or shifts in a child’s development […] might either overwhelm the synergy of the child’s linguistic, motor and/or monitoring systems, or evoke such changes in how speech is processed and produced? [...] Starting around 2 years of age, there is a transition from a lexically driven, asyntactic production system to the development of a qualitatively different, grammatically governed system capable of generating syntactic plans for speech execution […]” (Bernstein Ratner, 1997, pp. 113/114)
Likewise, Bloodstein (2006) pointed to the facts that “early stuttering seldom occurs on one-word utterances; the earliest age at which stuttering is reported is 18 months, with the beginning of grammatical development; the age at which most onset of stuttering is reported, 2-5 years, coincides with the period during which children acquire syntax; considerable spontaneous recovery takes place at the time most children have mastered syntax; incipient stuttering is influenced by the length and grammatical complexity of utterances...” (p. 185)
What is the role of auditory feedback in the transition from asyntactic one- or two-word utterances to grammatical, connected speech? Van Riper (1971) believed that auditory feedback becomes less important because the self-monitoring of speech shifts from the auditory channel to the proprioceptive, tactile, and kinesthetic feedback channels (read more).
If speech monitoring requires identifying self-produced words to detect errors (see Section 1.4), then Van Riper was wrong. We don’t recognize our spoken words by feeling the articulatory movements (except for people with innate deafness, who are specifically trained to monitor their speech in this way). A behavioral experiment conducted by Lind et al. (2014) has supported this view. They covertly manipulated their participants’ auditory feedback in real time so that they said one thing but heard themselves saying something else. In most cases, the participants believed that they had said what they heard.
From a theoretical viewpoint as well, there is no reason to assume the existence of two different pathways for receptive language processing in the brain, one for self-produced speech and one for the speech of others. Normally, we perceive, identify, and understand our words, as well as the words of others, by hearing them. This view is supported by neuroimaging studies, which have shown that the processing of both, self-produced speech and the speech of others, is localized in nearly the same cortical areas (McGuire, Silbersweig, & Frith, 1996; Price et al., 1996).
During the babbling period, hearing self-produced sounds and syllables is essential because the child (or the child’s brain) must generate solid connections between articulatory movements and their acoustic results. Playfully, the child acquires motor programs (routines) to produce the sounds, sound conjunctions, and simple syllables of the native language. The next step is that the child learns to speak single words; that is, connections between semantic content and speech-motor programs are established.
As long as children produce only single words and short phrases, for which they have acquired stable motor programs, monitoring via auditory feedback may play a minor role (so far, Van Riper was right), not least because the child gets feedback from others. Through their listeners’ responses, children realize whether their short utterances were understood., and if a word is wrong or incomplete, listeners will correct the mistake. It is therefore not surprising that stuttering does not yet occur in this one-word and two-word period.
Things change when children start forming simple sentences. Now, auditory feedback becomes important again, for two reasons. First, incremental sentence planning requires keeping the words produced (not the words planned) in memory to properly complete the current sentence, and as Lind et al. (2014) have demonstrated, we know from auditory feedback what we have said.
Second, a speech error in a sentence must be detected and repaired immediately, otherwise the entire sentence becomes wrong or misleading. Accompanying automatic monitoring based on auditory feedback enables the detection of errors and their immediate repair by interrupting speech flow (see Section 2.1).
What is known about how auditory feedback is involved in speech control in young stuttering children? A study by Natke et al. (2004b) provides a suggestion: In the early period, children do not clearly distinguish between stressed and unstressed syllables. They speak all syllables relatively long, which implies that the duration of each syllable is controlled based on the auditory feedback of the syllable start (audio-phonatory coupling). With time, children learn to produce short, unstressed syllables, whose duration is no longer feedback-controlled, but feedforward-controlled by the speech rhythm. Only the duration of long (stressed) syllables is still controlled via auditory feedback. So, the speech rate becomes higher, and prosody becomes more adult-like.
Some children seem to exaggerate independence from auditory feedback. Natke et al. (2004b) found that stuttering children (2.1–5 years of age) produced longer vowel durations in long stressed syllables than normal fluent children. The authors conclude that children who stutter “not only learn to automate the production of short syllables, but that of long stressed syllables as well. Also long stressed syllables are produced in the absence of auditory control, whereas in non-stuttering persons, auditory control remains effective in these syllables.” (p. 3).
Naturally, children are not aware of doing something qualitatively new when they speak their first simple sentences; hence, it is not surprising that some of them have difficulty with that change. They may try to form sentences in the same ‘holistic’ way as they previously produced single words and short phrases, focusing only on the intended message and paying no attention to auditory feedback. In other words, they focus solely on what they want to say and pay no attention to what they have already said. But fluent, connected speech requires attention to both.
To sum it up in simple words, the control of connected speech requires attention in two directions: to the future—what you want to say—and to the past—what you have already said. Stuttering arises when a child directs too much attention to the future and too little to the past. After a child has repeatedly experienced stuttering, a further reason to direct attention to the future can come in addition: fear of upcoming stuttering. This increases the imbalance.
Chow and Chang (2017) found differences in brain structure between young children who persisted in stuttering and children who later eventually recovered from the disorder. These differences at an early stage of development suggest that no gradual chronification of stuttering takes place; instead, recovery or persistence seem to be predetermined, with external factors having little influence. Therefore, I will distinguish between the development of transient stuttering, on the one hand, and of persistent stuttering, on the other hand.
Brain development in young children interacts with learning, that is, with the development of behavioral routines and habits. A sometimes overlooked component of behavior is the allocation of attention or, in other words, of perceptual and processing capacities. For a complex behavioral routine, such as speaking, an adequate allocation of attention must be learned and automated together with the motor abilities. I think that this rather unconscious component of speech development is the crucial factor for the occurrence of childhood stuttering; details have been described above. The figure shows the hypothesized development of transient stuttering from the onset to the recovery.
Figure 8: The development of transient stuttering.
The deeper, more general cause of childhood stuttering seems to be an imbalance in the development of the attention system: a preponderance of attention to action, that is, to goals (top-down attention), at the cost of attention to passive perception, including attention to sensory feedback (bottom-up attention). This causes problems in speech development at the change from one-word utterances to connected speech, as described above.
Some empirical findings suggest an imbalance in the attention system. Alm (2004) pointed to a high number of dopamine D2 receptors in children at ages 2.5 to 3 in general. This may reflect a transient imbalance in the control of behavior and attention in favor of action, associated with a higher risk of stuttering at this age.
A suggestion is the lower fractional anisotropy in the left arcuate fasciculus in stuttering children as compared with their non-stuttering peers (Chow & Chang, 2017). This suggests a delayed maturation (myelination) of those fibers in stuttering children. Interestingly, the deficit was often greater in the children who eventually recovered from stuttering than in those who persisted (see Fig. 1, Clusters 1 and 2 in the study).
The arcuate fasciculus is a bundle of nerve fibers connecting auditory areas with pre-motor and motor areas. Delayed maturation of these fibers may result from less frequent activation, namely, when auditory information is less assessed and less used in motor control. A correlation between the activation of nerve fibers and fractional anisotropy was demonstrated in several studies (e.g., Bengtsson et al., 2005; Fiedls, 2010; Keller & Just, 2009; Scholz et al., 2009).
A further suggestion is an atypical functional connectivity between neuronal networks in children who stutter as compared with normal developed children (Chang et al., 2018). Functional connectivity between brain areas means that these areas tend to be activated or deactivated synchronously without the need for a structural connection.
Particularly, the hyper-connectivity between the ventral attention network (VAN, mainly responsible for bottom-up attention) and default mode network (DMN; see Fig. 5A in the aforementioned study) suggests an imbalance in the control of attention. DMN is a set of brain regions that are deactivated during goal-directed tasks; therefore, hyper-connectivity between DMN and VAN possibly means that VAN tends to be deactivated too during goal-directed tasks. Since VAN is responsible for the automatic processing of sensory feedback, deactivation of VAN during goal-directed tasks may result in poor processing of sensory feedback during goal-directed tasks.
Interestingly, Chang et al. (2018) even found reduced functional connectivity within the visual network in stuttering children, suggesting a general deficit in the involvement of sensory input in the control of behavior.
Late-onset stuttering following a psychological trauma (but not stuttering after a brain injury) were included in Figure 8 because the underlying mechanism might be similar to that in developmental stuttering, but the affected individuals seem to have no strong physiological predisposition for stuttering, especially not for persistent stuttering. In someone whose attention system is susceptible, strong negative emotions, distress, fear, or the aftermath of a trauma may also result in a misallocation of attention during speech and, with that, in stuttering. Complete recovery is often reached in such cases by supporting environment or by therapy, including psychotherapy (see Table 1 in Chang et al., 2010).
Spontaneous recovery from stuttering may be caused by a kind of unconscious learning effect: children eventually learn to adapt the allocation of their attention to the new demands of connected speech. This learning effect manifests in brain structure; see, e.g., the upward developmental trajectories of fractional anisotropy in the recovered group in Chow and Chang (2017) in Clusters 3, 5, and 6. This progress in the structural integrity of nerve fibers may result from learning. Keller and Just (2009) and Scholz et al. (2009) demonstrated that even a few weeks of practice in reading or juggling can enhance fractional anisotropy in the fibers activated by the task.
The assumption that most stuttering children eventually learn to adapt their attention allocation to the demands of connected speech and, with that, overcome the disorder doesn’t mean that everything works the same as in children who have never stuttered. The findings obtained by Chang et al. (2008, 2018) show some differences in brain structure between the two groups. However, Chang et al. (2018) also found that the functional connectivity between the default mode network, attention networks, and executive control networks was normalized in recovered children.
Van Riper wrote: “When the words are first learned, the auditory channel must be the one through which the essential information flows if the comparison of output with the interiorized model and the consequent reduction of error signals are to be accomplished. However, we need our ears for other important functions – for perceiving our own verbalized thoughts and the thoughts of others. It would be to burdensome if we always had to play our speech by ear – if we were eternally doomed to listen to each sound and syllable of each word to ensure its correctness. In our opinion, the human being, as he always does when overloaded, finds a shorter and easier way. In this case, he turns over the major responsibility for the monitoring of speech to another available information processing system – the kinesthetic-tactual-proprioceptive one – as soon as possible. This change, we believe, occurs as soon as the auditory system stops giving error signals; as soon as the motor sequences involved in word production seem to be able to be produced correctly without constant auditory scrutiny.” (p. 393)
Not only Van Riper but also other researchers, e.g., Adams (1974) and Perkins et al. (1976), assumed that, during speech development, the auditory feedback channel gradually loses influence on speech control, until, in adults, only tactile-proprioceptive feedback is used for purposes of control. “Speech dysfluencies, then, originate from auditory feedback not sufficiently being suppressed. This may lead to interferences and/or discoordinations between different feedback channels […].”
However, experiments conducted by Bauer, Jäncke, & Kalveram (1997) did not support interference models of stuttering. In these experiments, irregular tactile and proprioceptive feedback was artificially generated by mechanically disturbing the jaw movement while speaking. These disturbances neither changed speech-relevant parameters of the acoustic speech signal, nor differentiated between stutterers and non-stutterers.
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