Background: experimentally induced dyspnea of the work/effort type inhibits, in a top-down manner, the spinal transmission of nociceptive inputs (dyspnea-pain counterirritation). Previous studies have demonstrated that this inhibition can be assessed by measuring the nociceptive flexion reflex (RIII). However, its clinical application is limited because of the strong discomfort associated with the electrical stimuli required to elicit the RIII reflex. Study objectives: we examined whether the dyspnea-pain counterirritation phenomenon can be evaluated by measuring the effect of work/effort type dyspnea on the magnitude of laser-evoked brain potentials (LEPs). Methods: 10 normal male volunteers were studied (age: 19–30 years). LEPs were elicited using a CO2 laser stimulator delivering 10- to 15-ms stimuli of 6 ± 0.7 W over a 12.5 mm2 area. The EEG was recorded using nine scalp channels. Non-nociceptive somatosensory-evoked potentials (SEPs) served as control. LEPs and SEPs were recorded before, during, and after 10 min of experimentally induced dyspnea [inspiratory threshold loading (ITL)]. Results: pain caused by the nociceptive laser stimulus was mild. ITL consistently induced dyspnea, mostly of the “excessive effort” type. Amplitude of the N2-P2 wave of LEPs decreased by 37.6 ± 13.8% during ITL and was significantly correlated with the intensity of dyspnea [ r = 0.66, CI 95% (0.08–0.92, P = 0.0319)]. In contrast, ITL had no effect on the magnitude of non-nociceptive SEPs. Discussion: experimentally induced dyspnea of the work/effort type reduces the magnitude of LEPs. This reduction correlates with the intensity of dyspnea. The recording of LEPs could constitute a clinically applicable approach to assess the dyspnea-pain counterirritation phenomenon in patients.
