Key result
Experimental air hunger significantly attenuated the N2-P2 amplitude of laser-evoked potentials by 22.6% compared to controlled breathing alone, suggesting a central mechanism for dyspnea-induced analgesia.
Why the study?
Does experimentally induced air hunger attenuate laser-evoked brain potentials in healthy volunteers?
Does experimentally induced air hunger attenuate laser-evoked brain potentials in healthy volunteers?
Experimental air hunger attenuates laser-evoked brain potentials, providing a neurophysiological substrate for the central nature of dyspnea-induced analgesia.
Answers are grounded in this paper and cite their sources.
Supports central dyspnea analgesia mechanisms in volunteers; hypothesis-generating for clinical translation, not yet practice-changing.
Dyspnea and pain share several characteristics and certain neural networks and interact with each other. Dyspnea-pain counter-irritation consists of attenuation of preexisting pain by intercurrent dyspnea and has been shown to have neurophysiological correlates in the form of inhibition of the nociceptive spinal reflex RIII and laser-evoked potentials (LEPs). Experimentally induced exertional dyspnea inhibits RIII and LEPs, while "air hunger" dyspnea does not inhibit RIII despite its documented analgesic effects. We hypothesized that air hunger may act centrally and inhibit LEPs. LEPs were obtained in 12 healthy volunteers (age: 21-29) during spontaneous breathing (FB), ventilator-controlled breathing (VC) tailored to FB, after inducing air hunger by increasing the inspired fraction of carbon dioxide -FiCO2- (VCCO2), and during ventilator-controlled breathing recovery (VCR). VCCO2 induced intense dyspnea (visual analog scale = 63% ± 6% of full scale, p < 0.001 vs. VC), predominantly of the air hunger type. VC alone reduced the amplitude of the N2-P2 component of LEPs (Δ = 24.0% ± 21.1%, p < 0.05, effect-size = 0.74) predominantly through a reduction in P2, and the amplitude of this inhibition was further reduced by inducting air hunger (Δ = 22.6% ± 17.9%, p < 0.05, effect-size = 0.53), predominantly through a reduction in N2. Somatosensory-evoked potentials (SEPs) were not affected by VC or VCCO2, suggesting that the observed effects are specific to pain transmission. We conclude that air hunger interferes with the cortical mechanisms responsible for the cortical response to painful laser skin stimulation, which provides a neurophysiological substrate to the central nature of its otherwise documented analgesic effects.
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Dangers et al. (2015) studied Healthy volunteers (n=12). Experimental air hunger (ventilator-controlled breathing with CO2 stimulation) vs. Ventilator-controlled breathing (VC) alone was evaluated on Amplitude of the N2-P2 component of laser-evoked potentials (LEPs) (Cohen's d 0.53, p=<0.05). Experimental air hunger significantly attenuated the N2-P2 amplitude of laser-evoked potentials by 22.6% compared to controlled breathing alone, suggesting a central mechanism for dyspnea-induced analgesia.
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