CONICET | Buscador de Institutos y Recursos Humanos

Experimental models of muscle pain in humans are crucial for understanding pain mechanisms.Commonly used models require invasive procedures (e.g. injection of algesic substances) or take a considerable time to develop (e.g. delayed onset muscle soreness). We recently developed a new experimental muscle pain model based on deep heat stimulation of the muscle using shortwave diathermy (SWD) [1]. The model is projected as a non-invasive, reliable and safe alternative to existing muscle pain models. However, its ability to induce relevant changes in sensorimotor processing has not yet been investigated. Thus, the aim of the present study was to assess electrophysiological changes in motor preparation during muscle pain.SWD was induced in the wrist extensor muscle group of the right arm of sixteen healthyvolunteers using two rectangular radiofrequency applicators. Irradiation intensity was fixed at a constant value, and SWD was applied until tolerance threshold for heat pain was reached. Quantitative evaluation of muscle soreness was performed through assessment of pressure pain thresholds (PPT) over extensor carpi radialis brevis (ECRB) muscles in both arms at baseline, and then 0, 30 and 60 minutes after SWD.Assessment of electrophysiological changes in motor preparationVolunteers performed two blocks of 25 ballistic wrist flexion movements executed as rapidly as possible with each arm, with an interval of 10 to 15 s between movements. The first block of flexions was performed right after application of SWD, whereas the second block was performed 30 min after SWD.Movements were cued by two beep sounds, the first one indicating to prepare for the upcoming task, and the second one to signal the actual movement onset, 2.5 s after the first one. Continuous electroencephalography (EEG) was recorded from C3, Cz, and C4, referenced to the right ear, accordingto the 10-20 international system. Electromyography (EMG) was recorded from the extensor muscle group of the dominant and non-dominant arm. EMG signals were used for calculation of movement onset and amplitude. All signals were amplified (gain: 24) and sampled at 2000 Hz.Data analysis and statisticsEEG signals were down-sampled (500 Hz) and digitally filtered between 0.25 Hz and 30 Hz using an 8th order zero-phase bandpass Butterworth filter. EMG signals were digitally filtered between 1 Hz and 100 Hz using an 8th order zero-phase bandpass Butterworth filter. EMG was fully rectified, and the envelope was extracted using the Hilbert transform. Recordings were segmented into 3.5-s trials, from 2.5 s before movement onset to 1 s after movement onset. EEG trials were averaged to extract movement related cortical potentials (MRCPs). A 2-way repeated measures ANOVA (with factors time and arm) was used toevaluate differences in PPT, calculated as percentage of change from baseline. A point-by point, mixed-model ANOVA was performed to evaluate differences in EMG and MRCP amplitude between arms for each time point, and a clustersize-based permutation testing approach was used to control for multiple comparisons. P values smaller than 0.05 were regarded as statistically significant.ResultsSWD evoked localized muscle pain/soreness in the wrist extensor muscle group and a decrease of PPT in the treated arm compared with the control arm that lasted for at least 60 minutes (p = 0.008). The cluster-based permutation tests revealed differences in MRCP amplitudes at C3 between arms around 1 s before movement onset at 0 and 30 min (p < 0.05), whereas no differences were found in EMG amplitudes.ConclusionsThe experimental pain model based on SWD induced changes in MRCP amplitudes, suggesting electrophysiological changes in motor preparation. Further work is required in order to fully describe the effects of changes in the model parameters (e.g. SWD intensity, application time, type of applicator) and the possibility of applying the model to other muscles (e.g. in the lower limb).