Given our assumptions about transient stuttering in the last section are true, then the question arises: Why does a minority of the children affected by stuttering not learn to adapt their attention to the demands of connected speech? A twofold cause seems to be responsible for that: (1) an imbalance in the attention system, similar as in transient stuttering, and (2) a deficit in central auditory processing, probably not present in transient stuttering. Perhaps both factors are related to each other or interact with each other. The development of persistent stuttering is sketched in Figure 20:
A finding by Chow and Chang (2017) which distinguished the group of stuttering children who eventually persisted from the group that eventually recovered is an initially (i.e., in the youngest children) higher FA value and its abnormal, stagnating or descending developmental trajectory in the thalamic radiation (see Fig. 2, Clusters 8, 9, and 10 in the study). These findings can hardly be explained as a consequence of stuttering because the differences are greatest in the youngest children. Since the thalamus plays a central role in attention regulation, the findings may be related to an abnormal development of the attention system.
Likewise, an anomalous functional connectivity between the attention networks and the default mode network (DMN) particularly in children who eventually persisted in stuttering (Fig. 3 in Chang et al ., 2018) indicates problems in the attention system in these children, however, the problems seem to partly differ from those in children with transient stuttering. Normal development proceeds in the way that other brain networks segregate from the DMN with age. Thus, the hyperconnectivity between VAN and DMN in children with transient stuttering (mentioned in the last section) can be interpreted as a delay in development which is partly overcome, partly compensated in the course of recovery. In children who persist in stuttering, by contrast, the connectivity between VAN and DMN and also between dorsal attention network and DMN is mainly reduced, suggesting a premature segregation of the networks in these children. This may have negative consequences for the further development of the attention system or for its integration in the control of behavior.
In addition, there are many behavioral studies in which deficits in attention regulation became apparent in PWS (see Section 3.31). Findings indicate that stutterers, on average, are less efficient in attention regulation, less able to divide attention under dual-task conditions, less able to quickly shift attention and to suppress a planned motor action. For example, Eggers, De Nil, and Van den Bergh (2012) concluded that the orienting network important for the allocation of attention appears to be less efficient in children who stutter, and Kaganovich, Hampton Wray, and Weber-Fox (2010) concluded from an examination of auditory processing in preschool-aged children who stutter, that stuttering may be associated with less efficient attention allocation.
Further, stutterers are more prone to exhibit attention disorders (symptoms of ADHD, particularly hyperactivity and impulsivity – see Section 3.3.1). Interestingly, both, persistent developmental stuttering and ADHD are more often diagnosed in males than in females (for ADHD, see Ramtekkar et al., 2010), which can be taken as a suggestion that the Factor 1 – especially by its components hyperactivity and impulsivity – is responsible for the greater prevalence of persistent stuttering in males
A central assumption of the attention allocation theory of stuttering is an imbalance between two components of behavioral control: between (1) internally initiated goal-directed action, controlled by the will, and associated with selective (top-down) attention, and (2) externally initiated re-action based on sensory input including sensory feedback, and more depending on non-selective (bottom-up) attention. A finding consistent with that central assumption is a heightened FA in the frontal aslant tract linking SMA to Broca’s area (Kronfeld-Duenias et al., 2016). The FA values of some subregions of the left frontal aslant tract were negatively correlated with speech fluency. Since the SMA is responsible for the voluntary control of behavior (after the model proposed by Goldberg, 1985; see also Section 2.1.1), we can interpret this finding as the manifestation of an overly strong influence of voluntary control on speech production in stutterers. A further finding points to the same direction: Xuan et al. (2012) found increased activation in the dorsolateral prefrontal cortex in adult males who stutter. They conclude: “Increased activity or activation in these prefrontal areas appears to reflect increased attention to action or increased attempts to deal with stuttering.”
Let us now look at the second, additional causal factor which seems to play a role in persistent stuttering: There are many empirical findings of deficits in the processing of non-linguistic and linguistic acoustic stimuli in stutterers, including the processing of the auditory feedback of speec – see Section 3.3.2. Unfortunately, there are few data about differences between those who persisted in stuttering and those who recovered in terms of auditory processing. The only study I know is that by Howell, Davis, and Williams (2006). They compared children of both groups in a backward-masking task the performance of which is assumed to reflect the operation of central auditory processing. They found an appropriately 10 decibel higher mean backward-masking threshold in the persistent group, i.e., the probe tone needed to be about 10dB louder on average for these children to hear it prior to the masking noise. The group difference was statistically significant, but there was a high variability in the persistent group, thus the authors conclude that an auditory deficit may be sufficient, but not necessary, for the disorder to persist.
In a preceding study, Howell et al, (2000) had found a higher backward-masking threshold on average in stuttering children as compared to normal fluent controls, with that threshold being positively correlated with stuttering frequency in the stuttering group; that is, the poorer central auditory processing, the greater stuttering frequency. A relationship between deficits in auditory processing and stuttering frequency or severity was found also in other studies (e.g., Beal et al., 2010, 2011Jansson-Verkasalo et al., 2014; Kikuchi et al., 2017; Liotti et al., 2010). Given that stuttering severity in children is (1) a predictor of eventual recovery or persistence (as concluded by Howell and Davis, 2011) and that (2) stuttering severity is related to central auditory processing, then we can assume that also auditory processing in young stuttering children can predict persistence or recovery. This hypothesis is consistent with the results of Howell, Davis, and Williams (2006) reported above and can be tested in a longitudinal study.
There are some further findings suggesting that a deficit in central auditory processing is the factor which distinguishes transient and persistent developmental stuttering: Usler and Weber-Fox (2015) as well as Mohan and Weber (2015) found differences between children with persistent stuttering and those who recovered in the processing of acoustically presented linguistic stimuli. Chow and Chang (2017) found a structural deficit (lower FA) in the splenium (the posterior part of the corpus callosum) in children who eventually persisted in stuttering, but not in those who eventually recovered (Fig. 1, Cluster 4 in the study). The affected fibers probably connect bilateral temporal regions (Kuvazeva, 2013), and lower FA may be related to less effective labor division between the hemispheres in auditory processing (callosal fibers often have inhibitory function, such that an activation in one hemisphere inhibits the homologous area in the other hemisphere).
The difference in FA in the mentioned Cluster 4 in Chow and Chang (2017) is great already with the youngest children, and there is no much overlap between the persistent group, on one hand, and the recovered and the control group, on the other hand. Therefore, the structural deficit in the splenium can hardly be a consequence of stuttering (while we can assume this when structural abnormalities grow with the duration of stuttering). Interestingly, Chow, Liu, Bernstein Ratner, and Braun found a strong relation between reduced FA in the splenium and stuttering severity in adults who stutter (unpublished study, presented at the 2014 ASHA Convention).
The theory that transient and persistent developmental stuttering are in core the same disorder, and that persistence is caused by one or more additional factors has already been proposed by Ambrose, Cox, and Yairi (1997) in a study of the genetic basis of persistence and recovery. They write: “ It was found that recovery or persistence is indeed transmitted, and further, that recovery does not appear to be a genetically milder form of stuttering, nor do the two types of stuttering appear to be genetically independent disorders. Data are most consistent with the hypothesis that persistent and recovered stuttering possess a common genetic etiology, and that persistence is, in part, due to additional genetic factors.”