Neural anomaly and reorganization in speakers who stutter

Abstract

Objectives:The aim of the current study was to differentiate between neural activity that represents neural anomalies that are responsible for persistent developmental stuttering (PDS) from the activity that is a result of compensating for stuttering. This was done by investigating alterations to the intrinsic functional architecture of speech-language processes of patients with PDS before and after a short-term intervention. Methods:The resting-state functional connectivity (RSFC) and cortical thickness were examined before and after the intervention. The structural data were used to validate the functional results. Fifteen stuttering patients who received intervention (PDSϩ), 13 stuttering patients who did not receive intervention (PDSϪ), and 13 fluent controls participated.Results: Before the intervention, both groups of PDS patients showed significant RSFC and cortical thickness reductions in the left pars-opercularis (PO) and RSFC increases in the cerebellum, as compared to fluent controls. The intervention was effective in reducing stuttering in PDSϩ patients and lowering their RSFC in the cerebellum to the level of fluent controls. The intervention effect was specific to the PDSϩ group (it was not evident in the PDSϪ group). The intervention did not change RSFC and cortical thickness in the left PO, which remained at its preintervention level. Conclusions:The results suggest that the left PO is a locus where the intrinsic functional architecture of speech-language processes is altered in PDS patients, suggesting an etiologic role of this region in PDS. The cerebellum showed intervention-induced neural reorganization, suggesting a compensatory response when stuttering occurs. Neurology ® 2012;79:625-632 GLOSSARY AFNI ϭ Analysis of Functional NeuroImages; BA ϭ Brodmann area; EPI ϭ echoplanar image; IC ϭ independent component; ICA ϭ independent component analysis; IFC ϭ inferior frontal cortex; MFG ϭ middle frontal gyrus; OASES ϭ Overall Assessment of the Speaker's Experience of Stuttering; PDS ϭ persistent developmental stuttering; PDS؊ ϭ stuttering patients who did not receive intervention; PDS؉ ϭ stuttering patients who received intervention; PO ϭ pars-opercularis; ROI ϭ region of interest; RSFC ϭ resting-state functional connectivity; SMA ϭ supplementary motor area; SSI-3 ϭ Stuttering Severity Instrument version III; TE ϭ echo time; TR ϭ repetition time.

Auditory‐motor adaptation is reduced in adults who stutter but not in children who stutter

“…The question remains as to what deficient neural substrates underlie these behavioral results. A growing body of evidence suggests that stuttering is associated with network‐level deficits in both cortico‐cortical loops and cortico‐subcortical loops rather than an isolated deficit in one specific brain region (Cai et al., ; Lu et al., ; Neef, Anwander, & Friederici, ). Studies on neurotypical adults have shown that cortico‐subcortical loops are heavily involved in sensorimotor integration (Doyon, Penhune, & Ungerleider, ; Doyon et al., ; Hardwick, Rottschy, Miall, & Eickhoff, ).…”

Behavioral and multimodal neuroimaging evidence for a deficit in brain timing networks in stuttering: a hypothesis and theory

“…Ingham et al (2012) examined speech during oral reading and monologs as well as rest, finding that PWS exhibited increased cerebellar activity which was negatively associated with stuttering, indicating that the ETN may indeed be compensating for the ITN. A similar study, examined resting state functional connectivity of PWS before and after speech therapy in stuttering and non-stuttering adults (Lu et al, 2012). These authors found increased resting-state-functional-connectivity between the midline CB and a network of regions (comprised of the medial frontal gyrus, the SMA and the left IFG) at rest for PWS relative to PWDS.…”

“…For the PWS who received intervention as compared to the PWS who did not receive intervention (and PWDS), the resting-state-functional-connectivity in the midline CB returned to normal levels and was correlated with an increase in fluency. As such, Lu et al (2012) suggested the CB was likely compensating in stuttering. In addition to these, other studies have associated the CB with compensatory activation in PWS (e.g., De Nil et al, 2008; Watkins et al, 2008).…”

“…In particular, the right IFG may only become active when a task is more demanding. That is to say, the difficulty of compensating for deficits in internal timing by external timing regions might account for why there was over-activation of only the CB during speech, but not the right IFG during rest in PWS (Lu et al, 2012). A second, though not mutually exclusive explanation is that while the CB is able to compensate for timing deficits, its ability to do so is limited.…”

Anterior capsulotomy improves persistent developmental stuttering with a psychiatric disorder: a case report and literature review

“…All these studies show that there are association fibers between the frontal operculum and the vPFC. The left pars opercularis is where the intrinsic functional architecture of speech–language processes are altered in PDS patients 22. Therefore, an anterior capsulotomy may affect the left pars opercularis through the vPFC and the association fibers between the vPFC and the pars opercularis, which are involved in the language system.…”