Differential Corticomotor Excitability Responses to Hypertonic Saline-Induced Muscle Pain in Forearm and Hand Muscles

Experimental muscle pain inhibits corticomotor excitability (CE) of upper limb muscles. It is unknown if this inhibition affects overlapping muscle representations within the primary motor cortex to the same degree. This study explored CE changes of the first dorsal interosseus (FDI) and extensor carpi radialis (ECR) muscles in response to muscle pain. Participants (n=13) attended two sessions (≥48 hours in-between). Hypertonic saline was injected in the ECR (session one) or the FDI (session two) muscle. CE, assessed by transcranial magnetic stimulation (TMS) motor-evoked potentials (MEPs), was recorded at baseline, during pain, and twenty minutes postinjection together with pain intensity ratings. Pain intensity ratings did not differ between the two pain sites (p=0.19). In response to FDI muscle pain, the MEPs of the FDI muscle were reduced at 2 and 4 min postinjection (p≤0.03), but not after ECR muscle pain. No significant MEP change was detected for the ECR muscle (p=0.62). No associations between MEPs and pain intensity were found (p>0.2). The present results indicate that the output from overlapping cortical representations of two muscles differentially adapts to acute muscle pain.

Acute muscle pain alters corticomotor output of the affected muscle stronger than a synergistic, ipsilateral muscle

Aims Muscle pain affects corticomotor areas representing the affected muscle, by changing the size of representation and reduces the corticospinal output as assessed by transcranial magnetic stimulation (TMS). Less work has been done to understand how pain in one muscle group may affect synergistic ipsilateral muscles distal to the pain. This study aimed to explore the effects of acute extensor carpi radialis (ECR) muscle pain on TMS motor-evoked potentials (MEPs) of the ECR and the first dorsal interosseus (FDI) muscle, which are known to strongly overlap within the corticomotor area. Methods Eight healthy volunteers (1 woman) were injected with hypertonic saline (5.8%, 0.5 mL) into the ECR muscle. Pain intensity was assessed by the visual analogue scale (VAS) every minute for 10 min. TMS was applied at 120% of ECR resting motor threshold, and MEPs were acquired from the ECR and the FDI muscles. At baseline, 10 TMS pulses were delivered. Temporal mapping of ECR and FDI MEPs over 10 min duration was performed by delivering 100 single-pulses of TMS, at 6 s interstimulus-interval. The MEPs for each muscle were averaged at baseline, peak-pain (1 –2 min epoch), and 10 min post-injection Results Pain intensity reduced significantly at 10 min postinjection as compared to peak-pain (P = 0.011). Further, one-way repeated measures analysis of variance revealed that ECR MEPs were altered at peak-pain compared to baseline (P > 0.05), but not 10 min post-injection (P > 0.05). Baseline and 10 min post-injection of ECR MEPs did not differ significantly (P = 0.67). The MEPs of the FDI muscle did not show a similar alteration over time (P = 0.1). Conclusions Despite the overlap between ECR and FDI representations, acute muscle pain of the ECR only significantly altered cortical excitability of the ECR muscle representation.

A single bout of aerobic exercise promotes motor cortical neuroplasticity

Regular physical activity is associated with enhanced plasticity in the motor cortex, but the effect of a single session of aerobic exercise on neuroplasticity is unknown. The aim of this study was to compare corticospinal excitability and plasticity in the upper limb cortical representation following a single session of lower limb cycling at either low or moderate intensity, or a control condition. We recruited 25 healthy adults to take part in three experimental sessions. Cortical excitability was examined using transcranial magnetic stimulation to elicit motor-evoked potentials in the right first dorsal interosseus muscle. Levels of serum brain-derived neurotrophic factor and cortisol were assessed throughout the experiments. Following baseline testing, participants cycled on a stationary bike at a workload equivalent to 57% (low intensity, 30 min) or 77% age-predicted maximal heart rate (moderate intensity, 15 min), or a seated control condition. Neuroplasticity within the primary motor cortex was then examined using a continuous theta burst stimulation (cTBS) paradigm. We found that exercise did not alter cortical excitability. Following cTBS, there was a transient inhibition of first dorsal interosseus motor-evoked potentials during control and low-intensity conditions, but this was only significantly different following the low-intensity state. Moderate-intensity exercise alone increased serum cortisol levels, but brain-derived neurotrophic factor levels did not increase across any condition. In summary, low-intensity cycling promoted the neuroplastic response to cTBS within the motor cortex of healthy adults. These findings suggest that light exercise has the potential to enhance the effectiveness of motor learning or recovery following brain damage.

Rectification of the EMG Signal Impairs the Identification of Oscillatory Input to the Muscle

Rectification of EMG signals is a common processing step used when performing electroencephalographic–electromyographic (EEG–EMG) coherence and EMG–EMG coherence. It is well known, however, that EMG rectification alters the power spectrum of the recorded EMG signal (interference EMG). The purpose of this study was to determine whether rectification of the EMG signal influences the capability of capturing the oscillatory input to a single EMG signal and the common oscillations between two EMG signals. Several EMG signals were reconstructed from experimentally recorded EMG signals from the surface of the first dorsal interosseus muscle and were manipulated to have an oscillatory input or common input (for pairs of reconstructed EMG signals) at various frequency bands (in Hz: 0–12, 12–30, 30–50, 50–100, 100–150, 150–200, 200–250, 250–300, and 300–400), one at a time. The absolute integral and normalized integral of power, peak power, and peak coherence (for pairs of EMG signals) were quantified from each frequency band. The power spectrum of the interference EMG accurately detected the changes to the oscillatory input to the reconstructed EMG signal, whereas the power spectrum of the rectified EMG did not. Similarly, the EMG–EMG coherence between two interference EMG signals accurately detected the common input to the pairs of reconstructed EMG signals, whereas the EMG–EMG coherence between two rectified EMG signals did not. The frequency band from 12 to 30 Hz in the power spectrum of the rectified EMG and the EMG–EMG coherence between two rectified signals was influenced by the input from 100 to 150 Hz but not from the input from 12 to 30 Hz. The study concludes that the power spectrum of the EMG and EMG–EMG coherence should be performed on interference EMG signals and not on rectified EMG signals because rectification impairs the identification of the oscillatory input to a single EMG signal and the common oscillatory input between two EMG signals.