Our meta-analysis suggests that the G allele of AR StuI polymorphism might be a potential risk factor for AGA, especially in white populations. However, we did not find any obvious association of the CAG and GGC triplet-repeat polymorphisms of the AR gene with risk for AGA.

The cerebellum has been implicated in the feedforward control of speech production. However, the role of the cerebellum in the feedback control of speech production remains unclear. To address this question, the present event‐related potential study examined the behavioral and neural correlates of auditory feedback control of vocal production in patients with spinocerebellar ataxia (SCA) and healthy controls. All participants were instructed to produce sustained vowels while hearing their voice unexpectedly pitch‐shifted −200 or −500 cents. The behavioral results revealed significantly larger vocal compensations for pitch perturbations in patients with SCA relative to healthy controls. At the cortical level, patients with SCA exhibited significantly smaller cortical P2 responses that were source localized in the right superior temporal gyrus, primary auditory cortex, and supramarginal gyrus than healthy controls. These findings indicate that reduced brain activity in the right temporal and parietal regions are significant neural contributors to abnormal auditory‐motor processing of vocal pitch regulation as a consequence of cerebellar degeneration, which may be related to disrupted reciprocal interactions between the cerebellum and cortical regions that support the top‐down modulation of auditory‐vocal integration. These differences in behavior and cortical activity between healthy controls and patients with SCA demonstrate that the cerebellum is not only essential for feedforward control but also plays a crucial role in the feedback‐based control of speech production.

Background: This study combined neuromechanical modeling analysis, muscle tone measurement from mechanical indentation and electrical impedance myography to assess the neural and peripheral contribution to spasticity post stroke at wrist joint. It also investigated the training effects and explored the underlying mechanism of radial extracorporeal shock wave (rESW) on spasticity.Methods: People with first occurrence of stroke were randomly allocated to rESW intervention or control group. The intervention group received one session of rESW therapy, followed by routine therapy which was the same frequency and intensity as the control group. Outcome measures were: (1) NeuroFlexor method measured neural component (NC), elastic component (EC) and viscosity component (VC), and (2) myotonometer measured muscle tone (F) and stiffness (S), (3) electrical impedance myography measured resistance (R), reactance (X) and phase angle (θ); (4) modified Asworth scale; (5) Fugl Meyer Upper limb scale. All outcome measures were recorded at baseline, immediately post rESW and at 1-week follow-up. The differences between the paretic and non-paretic side were assessed by t-test. The effectiveness of rESW treatment were analyzed by repeated-measures one-way analysis of variance (ANOVA) at different time points.Results: Twenty-seven participants completed the study. NC, EC, and VC of the Neuroflexor method, F and S from myotonometer were all significantly higher on the paretic side than those from the non-paretic side. R, X, and θ from electrical impedance were significantly lower on the paretic side than the non-paretic side. Immediately after rESW intervention, VC, F, and S were significantly reduced, and X was significantly increased. The clinical scores showed improvements immediate post rESW and at 1-week follow-up.Conclusions: The observed changes in upper limb muscle properties adds further support to the theory that both the neural and peripheral components play a role in muscle spasticity. ESW intervention may be more effective in addressing the peripheral component of spasticity in terms of muscle mechanical properties changes. The clinical management of post stroke spasticity should take into consideration of both the neural and non-neural factors in order to identify optimal intervention regime.

The dorsolateral prefrontal cortex (DLPFC) has been implicated in auditory–motor integration for accurate control of vocal production, but its precise role in this feedback-based process remains largely unknown. To this end, the present event-related potential study applied a transcranial magnetic stimulation (TMS) protocol, continuous theta-burst stimulation (c-TBS), to disrupt cortical activity in the left DLPFC as young adults vocalized vowel sounds while hearing their voice unexpectedly shifted upwards in pitch. The results showed that, as compared to the sham condition, c-TBS over left DLPFC led to significantly larger vocal compensations for pitch perturbations that were accompanied by significantly smaller cortical P2 responses. Source localization analyses revealed that this brain activity pattern was the result of reduced activation in the left superior frontal gyrus and right inferior parietal lobule (supramarginal gyrus). These findings demonstrate c-TBS-induced modulatory effects of DLPFC on the neurobehavioral processing of vocal pitch regulation, suggesting that disrupting prefrontal function may impair top–down inhibitory control mechanisms that prevent speech production from being excessively influenced by auditory feedback, resulting in enhanced vocal compensations for feedback perturbations. This is the first study that provides direct evidence for a causal role of the left DLPFC in auditory feedback control of vocal production.