• A Romaniello, G Cruccu, A S McMillan, L Arendt-Nielsen, and P Svensson.
• Center for Sensory-Motor Interaction, Orofacial Pain Laboratory, Aalborg University, Fredrik Bajers Vej 7, D-3 9220, Aalborg S, Denmark.
• Brain Res. 2000 Nov 3; 882 (1-2): 120-7.

AbstractThe pathophysiology of many orofacial pain syndromes is still unclear. We investigated the effect of tonic muscle and skin pain on the excitability of the trigeminal motor pathways using transcranial magnetic stimulation (TMS). Motor evoked potentials (MEPs) were recorded in the masseter surface electromyogram (EMG). Magnetic pulses were delivered with a large coil at intensities 1.1 and 1.5 times the motor threshold, and for each intensity, MEPs were recorded at three different clenching levels: 15, 30 and 45% of maximum voluntary contraction (MVC). Baseline, pain and post-baseline recordings were compared in two sessions. Firstly, muscle pain was induced by infusion of hypertonic saline (5.8%) into the left masseter. Secondly, skin pain was induced by topical application of capsaicin (5%) on the left cheek. Muscle and skin pain did not induce significant effects on the amplitude or latency of the MEPs (ANOVAs: P>0.50). In both sessions, the amplitude of the MEPs increased with the increase of the clenching level and stimulus intensity (P<0.0001; P<0.005) whereas the latency was not significantly changed (P>0.05; P=0.11). Muscle pain was associated with an increase in the pre-stimulus EMG activity on the non-painful side compared with baseline (P<0.01), which could be due to compensatory changes in the activation of the painful muscle. The need for voluntary contraction to evoke MEPs in the masseter muscles and compensatory mechanisms both at the brainstem and cortical level might explain the lack of detectable modulation of MEPs. Nonetheless, the present findings did not support the so-called 'vicious cycle' between pain - central hyperexcitability - muscle hyperactivity.

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