Transcranial direct current stimulation (tDCS) has been used as a useful interventional brain stimulation technique to improve unilateral upper-limb motor function in healthy humans, as well as in stroke patients. Although tDCS applications are supposed to modify the interhemispheric balance between the motor cortices, the tDCS after-effects on interhemispheric interactions are still poorly understood. To address this issue, we investigated the tDCS after-effects on interhemispheric inhibition (IHI) between the primary motor cortices (M1) in healthy humans. Three types of tDCS electrode montage were tested on separate days; anodal tDCS over the right M1, cathodal tDCS over the left M1, bilateral tDCS with anode over the right M1 and cathode over the left M1. Single-pulse and paired-pulse transcranial magnetic stimulations were given to the left M1 and right M1 before and after tDCS to assess the bilateral corticospinal excitabilities and mutual direction of IHI. Regardless of the electrode montages, corticospinal excitability was increased on the same side of anodal stimulation and decreased on the same side of cathodal stimulation. However, neither unilateral tDCS changed the corticospinal excitability at the unstimulated side. Unilateral anodal tDCS increased IHI from the facilitated side M1 to the unchanged side M1, but it did not change IHI in the other direction. Unilateral cathodal tDCS suppressed IHI both from the inhibited side M1 to the unchanged side M1 and from the unchanged side M1 to the inhibited side M1. Bilateral tDCS increased IHI from the facilitated side M1 to the inhibited side M1 and attenuated IHI in the opposite direction. Sham-tDCS affected neither corticospinal excitability nor IHI. These findings indicate that tDCS produced polarity-specific after-effects on the interhemispheric interactions between M1 and that those after-effects on interhemispheric interactions were mainly dependent on whether tDCS resulted in the facilitation or inhibition of the M1 sending interhemispheric volleys.
Spasticity is a frequent chronic complication in individuals with spinal cord injury (SCI). However, the severity of spasticity varies in patients with SCI. Therefore, an evaluation method is needed to determine the severity of spasticity. We used a contusive SCI model that is suitable for clinical translation. In this study, we examined the feasibility of the swimming test and an EMG for evaluating spasticity in a contusive SCI rat model. Sprague-Dawley rats received an injury at the 8th thoracic vertebra. Swimming tests were performed 3 to 6 weeks after SCI induction. We placed the SCI rats into spasticity-strong or spasticity-weak groups based on the frequency of spastic behavior during the swimming test. Subsequently, we recorded the Hoffman reflex (H-reflex) and examined the immunoreactivity of serotonin (5-HT) and its receptor (5-HT2A) in the spinal tissues of the SCI rats. The spasticity-strong group had significantly decreased rate-dependent depression of the H-reflex compared to the spasticity-weak group. The area of 5-HT2A receptor immunoreactivity was significantly increased in the spasticity-strong group. Thus, both electrophysiological and histological evaluations indicate that the spasticity-strong group presented with a more severe upper motor neuron syndrome. We also observed the groups in their cages for 20 hours. Our results suggest that the swimming test provides an accurate evaluation of spasticity in this contusive SCI model. We believe that the swimming test is an effective method for evaluating spastic behaviors and developing treatments targeting spasticity after SCI.
Unilateral isometric muscle contractions increase motor-evoked potentials (MEPs) produced by transcranial magnetic stimulation not only in the contracting muscle but also in the resting contralateral homologous muscle. Corticospinal excitability in the M1 contralateral to the contracting muscle changes depending on the type of muscle contraction. Here, we investigated the possibility that corticospinal excitability in M1 ipsilateral to the contracting muscle is modulated in a contraction-type-dependent manner. To this end, we evaluated MEPs in the resting left flexor carpi radialis (FCR) during unilateral shortening, lengthening, and isometric muscle contractions of the right wrist flexors at 10, 20, and 30% of maximal isometric contraction force. To compare the effects of different unilateral contractions on MEPs between the contracting and resting sides, MEPs in the right FCR were recorded on two separate days. In a separate experiment, we investigated the contraction specificity of the crossed effect at the spinal level by recording H-reflexes from the resting left FCR during contraction of the right wrist flexors. The results showed that MEPs in the contracting right FCR were the smallest during lengthening contraction. By contrast, MEPs in the resting left FCR were the largest during lengthening contraction, whereas the H-reflex was similar in the resting left FCR during the three types of muscle contraction. These results suggest that different types of unilateral muscle contraction asymmetrically modulate MEP size in the resting contralateral homologous muscle and in the contracting muscle and that this regulation occurs at the supraspinal level.
Recent studies demonstrated that the corticospinal pathway is one of the key nodes for the feedback control of human standing and that the excitability is flexibly changed according to the current state of posture. However, it has been unclear whether this pathway is also involved in a predictive control of human standing. Here, we investigated whether the corticospinal excitability of the soleus (SOL) and tibialis anterior (TA) muscles during standing would be modulated anticipatorily when perturbation was impending. We measured the motor-evoked potential (MEP) induced by transcranial magnetic stimulation over the motor cortex at six stimulus intensities. Three experimental conditions were set depending on predictabilities about perturbation occurrence and onset: No perturbation, No Cue, and Cue conditions. In the Cue condition, an acoustic signal was given as timing information of perturbation. The slope of the stimulus–response relation curve revealed that the TA-MEP was enhanced when postural perturbation was expected compared to when the perturbation was not expected (No Perturbation vs. No Cue, 0.023 ± 0.004 vs. 0.042 ± 0.007; No Perturbation vs. Cue, 0.023 ± 0.004 vs. 0.050 ± 0.009; Bonferroni correction, p = 0.01, respectively). In addition, two-way analysis of variance (intensity × condition) revealed the main effect of condition (F(1,13) = 6.31, p = 0.03) but not intensity and interaction when the MEP amplitude of the Cue and No Cue conditions was normalized by that in No Perturbation, suggesting the enhancement more apparent when timing information was given. The SOL-MEP was not modulated even when perturbation was expected, but it slightly reduced due to the timing information. The results of an additional experiment confirmed that the acoustic cue by itself did not affect the TA- and SOL-MEPs. Our findings suggest that a prediction of a future state of standing balance modulates the corticospinal excitability in the TA, and that the additional timing information facilitates this modulation. The corticospinal pathway thus appears to be involved in mechanisms of the predictive control as well as feedback control of standing posture.
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