Short-latency afferent inhibition (SAI) and long-latency afferent inhibition (LAI) occur when the motor evoked potential (MEP) elicited by transcranial magnetic stimulation (TMS) is reduced by the delivery of a preceding peripheral nerve stimulus. The intra-individual variability in SAI and LAI is considerable, and the influence of sample demographics (e.g., age and biological sex) and testing context (e.g., time of day) is not clear. There are also no established normative values for these measures, and their reliability varies from study-to-study. To address these issues and facilitate the interpretation of SAI and LAI research, we pooled data from studies published by our lab between 2014 and 2020 and performed several retrospective analyses. Patterns in the depth of inhibition with respect to age, biological sex and time of testing were investigated, and the relative reliability of measurements from studies with repeated baseline SAI and LAI assessments was examined. Normative SAI and LAI values with respect to the mean and standard deviation were also calculated. Our data show no relationship between the depth of inhibition for SAI and LAI with either time of day or age. Further, there was no significant difference in SAI or LAI between males and females. Intra-class correlation coefficients (ICC) for repeated measurements of SAI and LAI ranged from moderate (ICC = 0.526) to strong (ICC = 0.881). The mean value of SAI was 0.71 ± 0.27 and the mean value of LAI was 0.61 ± 0.34. This retrospective study provides normative values, reliability estimates, and an exploration of demographic and testing influences on these measures as assessed in our lab. To further facilitate the interpretation of SAI and LAI data, similar studies should be performed by other labs that use these measures.

Neurotransmission is highly dependent on the availability of glucose-derived energy, although it is unclear how glucose availability modulates corticospinal and intracortical excitability as assessed via transcranial magnetic stimulation (TMS). In this double-blinded placebo-controlled study, we tested the effect of acute glucose intake on motor-evoked potential (MEP) recruitment curves, short-interval intracortical inhibition (SICI), short-latency afferent inhibition (SAI) and long-latency afferent inhibition (LAI). Eighteen healthy males participated in four sessions. Session 1 involved acquisition of an individualized blood glucose response curve. This allowed measurements to be time-locked to an individualized glucose peak after consuming one of three drinks during the subsequent three sessions. Participants were administered a 300 mL concealed solution containing 75 g of glucose, sucralose, or water in separate sessions. Dependent measures were assessed at baseline and twice after drinking the solution. Secondary measures included blood glucose and mean arterial pressure. Corticospinal excitability and blood pressure increased following the drink across all treatments. No changes were observed in SICI, SAI or LAI. There was no rise in corticospinal excitability that was specific to the glucose drink, suggesting that acute changes in glucose levels do not necessarily alter TMS measures of corticospinal or intracortical excitability.

Electromyography (EMG)-based biofeedback has considerable potential as a mode of therapeutic exercise for individuals with motor impairments. Advances in technology now allow the delivery of biofeedback with cheap, compact computers and sensors. Reliable machine learning classification of EMG signals in real-time, which is a core component of many biofeedback systems, is also now easily accessible through various open-source software libraries. Despite this progress and the attention garnered by EMG biofeedback among researchers, broad clinical acceptance remains elusive. We aim to open this technology to a broader audience by proposing an accessible standard approach to the design and implementation of EMG-based biofeedback systems. We highlight important considerations when designing a system to deliver potent biofeedback, including maximizing motivation, minimizing constraints on sensor number or configuration, and maximizing replicability by other researchers. Based on relevant neuroscientific and technical literature, we recommend methods and procedures by which these goals can be achieved. Finally, we create and test a biofeedback system in a sample of both healthy and motor impaired volunteers. We found that the EMG biofeedback system supported accurate and stable control by healthy and impaired users and could be implemented with minimal access to coding expertise and an off-the-shelf EMG device. This work expands awareness of effective design principles for EMG biofeedback systems and will advance the state-of-the-art in this field.

It is unclear why specific individuals incur chronic symptoms following a concussion. This exploratory research aims to identify and characterize any neurophysiological differences that may exist in motor cortex function in post-concussion syndrome (PCS). Fifteen adults with PCS and 13 healthy, non-injured adults were tested. All participants completed symptom questionnaires, and transcranial magnetic stimulation (TMS) was used to measure intracortical and transcallosal excitability and inhibition in the dominant motor cortex. Cortical silent period (p = 0.02, g = 0.96) and ipsilateral silent period (p = 0.04, g = 0.78) were shorter in the PCS group compared to the control group which may reflect reduced GABA-mediated inhibition in PCS. Furthermore, increased corticomotor excitability was observed in the left hemisphere but not the right hemisphere. These data suggest that persistent neurophysiological differences are present in those with PCS. The exact contributing factors to such changes remain to be investigated by future studies. This study provides novel evidence of lasting neurophysiological changes in PCS.