5. The development of stuttering

5.1. Transient stuttering

Let us now look again at the development of the disorder and at the factors involved – factors that trigger the mechanism, and those that contribute to its maintenance or overcoming, respectively. Recent investigation of young stuttering children near the onset of the disorder (Chow and Chang, 2017) showed some differences in brain structure between children who eventually recovered from stuttering and those who persisted, as groups, even at this early stage of development. This suggests that no gradual chronification of stuttering takes place; recovery or persistence seem to be rather predetermined, with external factors having little influence. In this chapter, it is therefore distinguished between the development of transient stuttering, on one hand, and of persistent stuttering, on the other hand, Psychogenic stuttering is dealt with in the section on transient stuttering, because the physical predisposition for stuttering is rather low in these cases, and appropriate psychotherapy often leads to complete recovery.

Idiopathic stuttering is today regarded as a neurodevelopmental disorder, however, brain development especially in young children interacts with learning, i.e., with the development of behavioral routines and habits. An aspect of behavior often overlooked is the allocation of attention and, with that, of perceptual and processing capacity. For every more complex behavioral routine, and also for speaking, an adequate allocation of attention must be learned and automatized. In the present theory, it is assumed that just this rather unconscious aspect of behavioral control is the crucial factor in the development of stuttering. Figure 19 shows the development from onset to recovery (persistent stuttering is not included in this figure).

Theory of stuttering: transient developmental stuttering, causal and influencing factors

Figure 19: The development of transient stuttering.

The cause of childhood stuttering, in most cases, seems to be an imbalance in the development of the attention system; a preponderance of attention to to action, i.e., to goals (top-down), to the detriment of the attention to passive perception, including the attention to sensory feedback (bottom-up). This becomes problematic in speech development at the change from oneword utterances to connected speech and sentence production, when auditoy feedback and the sensory feedback of breathing must be more involved in speech control. The brain needs to know which constituents of a sentence have already been produced in order to correctly complete the sentence, and speech errors in a sentence must be detected immediately (which depends on auditory feedback; see Chapter 1). Breathing times must be included in the linguistic sequence at proper positions. Children naturally are not aware of changing behavior when they start forming sentences, and they cannot know that they need to change their attentional behavior.

There are some empirical findings suggesting an imbalance in the attention system: first, a high number of dopamine D2 receptors at age 2.5 to 3 (Alm 2004; Rothmond et al. 2012). Alm (2004) has assumed that a high dopamine reception in the basal ganglia immediately causes stutter-ing, but the high dopamine level may rather manifest an imbalance in behavioral and attentional control which may cause a higher risk of stuttering at this age.

A second,finding is a lower fractional anisotropy in the left arcuate fasciculus in children who stutter. as compared with their non-stuttering peers (Chow and Chang, 2017). This finding was, in part, more significant in children who eventually recovered from stuttering than in those who persisted (see Fig. 1, Clusters 1 and 2 in the study). Fractional anisotropy (FA) means the anisotropy of the diffusion of water molecules; it is a measure allowing to investigate the course of nerve fiber bundles in the brain and their structural features, e.g., the degree of myelination or ‘maturation’. Arcuate fasciculus is a bundle of nerve fibers connecting sensory cortical areas with premotor and motor areas. Lower FA can be interpreted as a delay in fiber maturation which, in turn, can result from less frequent activation of the fibers when sensory information is less involved in motor planning and -control (a correlation between the activation of nerve fibers and FA was shown in several studies, e.g., Bengtsson et al., 2005; Keller and Just, 2009; Scholz et al., 2009). The relationship between fiber activation and maturation/myelination is described more detailed in Section 4.1.

A further finding suggesting an imbalance in the attention system 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 of a structural connection. Particularly the hyperconnectivity between 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, thus hyperconnectivity between DMN and VAN means that also VAN is tendentially deactivated during goal-directed tasks. Since VAN is responsible for the automatic processing of sensory feedback, deactivation of VAN during goal-directed tasks means that sensory feedback tendentially is poorly processed during goal-directed tasks. Interestingly, Chang et al. (2018) even found a reduced functional connectivity in the visual network in stuttering children, suggest-ing a general deficit in the involvement of sensory input in the control of behavior.  

The most important trigger for the onset of childhood stuttering, after the present theory, is the child’s change to connected speech and sentence production. This idea is not new: Bloodstein (2006, p. 185) 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...”

Late-onset stuttering and the so called psychogenic stuttering were included in the scheme for transient stuttering (Fig. 19) because the underlying mechanism might be the same as in developmental stuttering, but indi-viduals affected seem to have no strong physical predisposition for stuttering, especially not for persistent stuttering. In a person whose attention system is susceptible, strong negative emotions, distress, fear, or the aftermath of a trauma may result in a misallocation of attention also during speech and by that in stuttering. Complete recovery is often reached in such cases by a supporting environment and/or by therapy, including psycho-therapy (see Table 1 in Chang et al.,2010).

Spontaneous recovery from stuttering is probably 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 and sentence production. This learning effect manifests in brain structure, see, e.g., the upward developmental trajectories of FA in the recovered group in Chow and Chang (2017) in the Clusters 3, 5, and 6. This progress in the structural integrity of nerve fibers may result from learning, as it was shown that even a few weeks of practice, e.g., in reading or in juggling, can result in enhanced FA values in the white matter of involved brain regions (Keller and Just, 2009; Scholz et al., 2009).

The assumption that most stuttering children eventually learn to adapt their attentional allocation to the demands of connected speech and, by that, overcome the disorder does not mean that all things function completely in the same way as in children who have never stuttered. The findings obtained by Chang et al. (2008, 2018) showed some differences in brain structure and -function between children who had recovered from stuttering and their normal developed peers. However,, Chang et al. (2018) found the functional connectivity especially between,default mode network, attention networks, and executive control networks to be normalized in recovered children.

 

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