15Accumulating evidence across species indicates that brain oscillations are superimposed 16 upon an aperiodic 1/# -like power spectrum. Maturational changes in neuronal oscillations 17 have not been assessed in tandem with this underlying aperiodic spectrum. The current study 18 uncovers co-maturation of the aperiodic component alongside the periodic components 19 (oscillations) in spontaneous magnetoencephalography (MEG) data. Beamformer-20 reconstructed MEG time-series allowed a direct comparison of power in the source domain 21 between 24 children (8.0 ± 2.5 years, 17 males) and 24 adults (40.6 ± 17.4 years, 16 males). 22Our results suggest that the redistribution of oscillatory power from lower to higher frequencies 23 that is observed in childhood does not hold once the age-related changes in the aperiodic 24 signal are controlled for. When estimating both the periodic and aperiodic components, we 25 found that power increases with age in the beta band only, and that the 1/# signal is flattened 26 in adults compared to children. These results suggest a pattern of co-maturing beta oscillatory 27 power with the aperiodic

There are widespread abnormalities in the structural architecture and functional organization of the brains of adults and children who stutter. These are evident not only in speech tasks, but also non-speech tasks. Future research should make greater use of functional neuroimaging and noninvasive brain stimulation, and employ structural methodologies that have greater sensitivity. Newly planned studies should also investigate sex differences, focus on augmenting treatment, examine moments of dysfluency and longitudinally or cross-sectionally investigate developmental trajectories in stuttering.

The fluent production of speech requires accurately timed movements. In this article, we propose that a deficit in brain timing networks is one of the core neurophysiological deficits in stuttering. We first discuss the experimental evidence supporting the involvement of the basal ganglia and supplementary motor area (SMA) in stuttering and the involvement of the cerebellum as a possible mechanism for compensating for the neural deficits that underlie stuttering. Next, we outline the involvement of the right inferior frontal gyrus (IFG) as another putative compensatory locus in stuttering and suggest a role for this structure in an expanded core timing-network. Subsequently, we review behavioral studies of timing in people who stutter and examine their behavioral performance as compared to people who do not stutter. Finally, we highlight challenges to existing research and provide avenues for future research with specific hypotheses.

Neuroimaging studies have shown that the neural mechanisms of motor imagery (MI) overlap substantially with the mechanisms of motor execution (ME). Surprisingly, however, the role of several regions of the motor circuitry in MI remains controversial, a variability that may be due to differences in neuroimaging techniques, MI training, instruction types, or tasks used to evoke MI. The objectives of this study were twofold: (i) to design a novel task that reliably invokes MI, provides a reliable behavioral measure of MI performance, and is transferable across imaging modalities; and (ii) to measure the common and differential activations for MI and ME with functional magnetic resonance imaging (fMRI) and magnetoencephalography (MEG). We present a task in which it is difficult to give accurate responses without the use of either motor execution or motor imagery. The behavioral results demonstrate that participants performed similarly on the task when they imagined vs. executed movements and this performance did not change over time. The fMRI results show a spatial overlap of MI and ME in a number of motor and premotor areas, sensory cortices, cerebellum, inferior frontal gyrus, and ventrolateral thalamus. MI uniquely engaged bilateral occipital areas, left parahippocampus, and other temporal and frontal areas, whereas ME yielded unique activity in motor and sensory areas, cerebellum, precuneus, and putamen. The MEG results show a robust event-related beta band desynchronization in the proximity of primary motor and premotor cortices during both ME and MI. Together, these results further elucidate the neural circuitry of MI and show that our task robustly and reliably invokes motor imagery, and thus may prove useful for interrogating the functional status of the motor circuitry in patients with motor disorders.