The distribution and reliability of TMS-evoked short- and long-latency afferent interactions

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.

The Number or Type of Stimuli Used for Somatosensory Stimulation Affected the Modulation of Corticospinal Excitability

Motor evoked potentials (MEPs) evoked by transcranial magnetic stimulation (TMS) a few milliseconds after this cortical activity following electrical stimulation (ES) result in an inhibition comparable to that by TMS alone; this is called short-latency afferent inhibition (SAI). Cortical activity is observed after mechanical tactile stimulation (MS) and is affected by the number of stimuli by ES. We determined the effects of somatosensory stimulus methods and multiple conditioning stimuli on SAI in 19 participants. In experiment 1, the interstimulus intervals between the conditioning stimulation and TMS were 25, 27 and 29 ms for ES and 28, 30 and 32 ms for MS. In experiment 2, we used 1, 2, 3 and 4 conditioning stimulations of ES and MS. The interstimulus interval between the ES or MS and TMS was 27 or 30 ms, respectively. In experiment 1, MEPs were significantly decreased in both the ES and MS conditions. In experiment 2, MEPs after ES were significantly decreased in all conditions. Conversely, MEPs after MS were significantly decreased after one stimulus and increased after four stimulations, indicating the SAI according to the number of stimuli. Therefore, the somatosensory stimulus methods and multiple conditioning stimuli affected the SAI.

Cortical Excitability and Connectivity in Patients With Brain Tumors

Background: Brain tumors can cause different changes in excitation and inhibition at the neuronal network level. These changes can be generated from mechanical and cellular alterations, often manifesting clinically as seizures.Objective/Hypothesis: The effects of brain tumors on cortical excitability (CE) have not yet been well-evaluated. The aim of the current study was to further investigate cortical–cortical and cortical–spinal excitability in patients with brain tumors using a more extensive transcranial magnetic stimulation protocol.Methods: We evaluated CE on 12 consecutive patients with lesions within or close to the precentral gyrus, as well as in the subcortical white matter motor pathways. We assessed resting and active motor threshold, short-latency intracortical inhibition (SICI), intracortical facilitation (ICF), short-latency afferent inhibition (SAI), long-latency afferent inhibition, cortical silent period, and interhemispheric inhibition.Results: CE was reduced in patients with brain tumors than in healthy controls. In addition, SICI, ICF, and SAI were lower in the affected hemisphere compared to the unaffected and healthy controls.Conclusions: CE is abnormal in hemispheres affected by brain tumors. Further studies are needed to determine if CE is related with motor impairment.

Influence of Brain-Derived Neurotrophic Factor Genotype on Short-Latency Afferent Inhibition and Motor Cortex Metabolites

The Met allele of the brain-derived neurotrophic factor (BDNF) gene confers reduced cortical BDNF expression and associated neurobehavioral changes. BDNF signaling influences the survival, development, and synaptic function of cortical networks. Here, we compared gamma-aminobutyric acid (GABA)ergic network activity in the human primary motor cortex (M1) between the Met (Val/Met and Met/Met) and non-Met (Val/Val) genotype groups. Short- and long-interval intracortical inhibition, short-latency afferent inhibition (SAI), and long-latency afferent inhibition were measured using transcranial magnetic stimulation (TMS) as indices of GABAergic activity. Furthermore, the considerable inter-individual variability in inhibitory network activity typically measured by TMS may be affected not only by GABA but also by other pathways, including glutamatergic and cholinergic activities; therefore, we used 3-T magnetic resonance spectroscopy (MRS) to measure the dynamics of glutamate plus glutamine (Glx) and choline concentrations in the left M1, left somatosensory cortex, and right cerebellum. All inhibitory TMS conditions produced significantly smaller motor-evoked potentials than single-pulses. SAI was significantly stronger in the Met group than in the Val/Val group. Only the M1 Glx concentration was significantly lower in the Met group, while the BDNF genotype did not affect choline concentration in any region. Further, a positive correlation was observed between SAI and Glx concentrations only in M1. Our findings provide evidence that the BDNF genotype regulates both the inhibitory and excitatory circuits in human M1. In addition, lower Glx concentration in the M1 of Met carriers may alter specific inhibitory network on M1, thereby influencing the cortical signal processing required for neurobehavioral functions.

RUNNING-INDUCED CHANGES IN H-REFLEX AMPLITUDES IN NON-TRAINED MEN

Effect of 5-weeks running training on modulation of the H-reflex amplitude on soleus muscle in non-trained men was studied. It was established that modulation of the H-reflex amplitude occurs in two phases. In the course of the first 3 weeks of running training (first phase) statistically significant (p < 0.05) increase in H-reflex amplitudes and the maximum H-reflex to the maximum M-response amplitudes ratio (10%) were registered. In contrast to the first phase, decrease in investigated parameters up to initial values were observed during the next 2 weeks of the training (second phase). An increase in the of the soleus H-reflex amplitude, is probably due to the enhanced drive in descending pathways, increased motoneuron excitability and changes in presynaptic Ia afferent inhibition, whereas decrease in the amplitude of the H-reflex might occurs presumably due to motor learning. Apparently, that the repetitive task, which automatically performed and controlled on a spinal or brainstem level can be reflected in the normalization and stabilization of the H-reflexes registered after running training in later period.