![]() On the one hand, rs-fMRI is free from confounds of task performance, particularly in participants who may present symptoms such as physical concomitants during speaking. One suitable approach to scrutinizing learning-induced neuroplasticity is the use of resting-state functional magnetic resonance imaging (rs-MRI). Here it is not the question whether the extensive speech training shapes speech related brain structures and dynamics, but which concrete networks are addressed. It is well established that extensive sensorimotor learning induces neuroplasticity 31. In the current study, this learning process was embedded in an intensive two-week on-site intervention and a one-year stand-alone speech training that required computer-assisted daily practice 30. ![]() One common approach to overcome these characteristic motor signs of stuttering is fluency shaping, a speech restructuring method that require individuals who stutter to learn a changed speech pattern. Speech production in stuttering is characterized by sound and syllable repetitions, sound prolongations and speech blocks, which can be accompanied by physical concomitants such as facial grimacing, head or limb movements. Taken together, findings give rise to different theories of stuttering, which is seen as a problem of sensorimotor integration and timing, either caused by a basal ganglia dysfunction or caused by a disconnection of cortical speech regions (Civier et al., 2013). Movement control engages the basal ganglia and the cerebellum, further crucial brain regions that show abnormal activity and connectivity in adults with persistent developmental stuttering 21, 24, 28, 29. In addition to irregular activity patterns, further imaging findings indicate white matter deficits 20– 24 in the dorsal language pathway 25, 26, the frontal motor pathway 26, 27 and interhemispheric connections between the sensorimotor cortices 19. Quantitative meta-analyses link stuttering to reduced left fronto-parieto-temporal speech network activity while greater speech fluency of affected individuals is associated with boosted co-activations of homologue right fronto-parietotemporal areas 16– 19. Neuroimaging studies provide much of the early evidence implicating particular brain regions in developmental stuttering 8. Thus, our understanding of neurophysiological mechanistic principles of stuttering and its neural remediation remains limited. However, especially in adults who experienced lifelong stuttering it is difficult to differentiate core neural deficits from stuttering-induced neural signatures, respectively, therapy-induced neuroplasticity from compensatory network activity. In developmental stuttering, a heritable speech fluency disorder 12 of unknown origin 13, 14, neuroimaging studies indicate aberrant brain activity and connectivity, in particular in brain structures that convey the abovementioned functions (for an overview see e.g. These networks incorporate speech planning 1, 2, sensorimotor integration 3– 6, articulatory convergence 7– 9, and the inhibition of competitive processes 10, 11. Taken together, structural and functional connectivity of the sensorimotor integration and inhibitory control network shape speech motor learning.įluent speech requires a complex interplay of multiple neuronal networks. We found a heightened negative correlation between stuttering severity and fractional anisotropy in the superior longitudinal fasciculus, and a heightened positive correlation between the psycho-social impact of stuttering and fractional anisotropy in the right frontal aslant tract. But, brain-behavior relationships changed. No alterations were found within white matter microstructure. Since we investigated task-free brain activity, we assume that our findings are not biased to network activity involved in compensation. The integration of the command-to-execution and auditory-motor pathway was strengthened. Specifically, two connections were strengthened, left laryngeal motor cortex and right superior temporal gyrus showed increased connectivity with the left inferior frontal gyrus. Improved fluency was accompanied by an increased synchronization within the sensorimotor integration network. Furthermore, we examined white matter metrics of major speech tracts. Here, we tested the impact of fluency-shaping on resting-state fMRI connectivity of the speech planning, articulatory convergence, sensorimotor integration, and inhibitory control network. Currently, it is unclear which functional domain is targeted by speech fluency interventions. Fluent speech requires multifunctional network formations. Developmental stuttering is a fluency disorder with anomalies in the neural speech motor system.
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