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Interactions Between Dyspnea and the Brain Processing of Nociceptive Stimuli: Experimental Air Hunger Attenuates Laser-Evoked Brain Potentials in Humans.

Dangers L, Laviolette L, Similowski T, Morélot-Panzini C - Front Physiol (2015)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Sorbonne Universités, University Pierre et Marie Curie Univ Paris 06, UMR_S 1158 "Neurophysiologie Respiratoire Expérimentale et Clinique" Paris, France ; Institut National de la Santé et de la Recherche Médicale, UMR_S 1158 "Neurophysiologie Respiratoire Expérimentale et Clinique" Paris, France ; Assistance Publique des Hôpitaux de Paris, Groupe Hospitalier Pitié-Salpêtrière Charles Foix, Service de Pneumologie et Réanimation Médicale (Département "R3S") Paris, France.

ABSTRACT
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.

No MeSH data available.


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Amplitude of the N2-P2 component of laser-evoked potentials (12 subjects). FB, free spontaneous breathing; VC, controlled breathing (ventilator); VCCO2, controlled breathing with CO2 stimulation; VCR, controlled breathing after removal of CO2 stimulation. Bars depict mean values, with indication of 1 standard deviation.
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Figure 3: Amplitude of the N2-P2 component of laser-evoked potentials (12 subjects). FB, free spontaneous breathing; VC, controlled breathing (ventilator); VCCO2, controlled breathing with CO2 stimulation; VCR, controlled breathing after removal of CO2 stimulation. Bars depict mean values, with indication of 1 standard deviation.

Mentions: The pain evaluated by the subjects at the laser perception threshold was 25 ± 13% of full scale on the pain VAS. Table 2 summarizes the LEPs amplitudes and latencies for all experimental conditions. A statistically significant attenuation of N2-P2 amplitude was observed during VC compared to FB (Δ = 24.0% ± 21.1%, p < 0.05, effect-size = 0.74) (Figures 3, 4). Further attenuation occurred during the VCCO2 condition (VC vs. VCCO2: Δ = 22.6% ± 17.9%, p < 0.05, effect-size = 0.53) (Figures 3, 4). Of note, the VC-associated reduction in N2-P2 was driven by reduction in P2 without significant change in N2, while the VCCO2-associated further reduction in N2-P2 was driven by a reduction in N2 without significant change in P2. We observed a trend to recovery between the VCCO2 and VCR conditions but not significant (VCCO2 vs. VCR: Δ = 32% ± 53%, ns effect-size = 0.36).


Interactions Between Dyspnea and the Brain Processing of Nociceptive Stimuli: Experimental Air Hunger Attenuates Laser-Evoked Brain Potentials in Humans.

Dangers L, Laviolette L, Similowski T, Morélot-Panzini C - Front Physiol (2015)

Amplitude of the N2-P2 component of laser-evoked potentials (12 subjects). FB, free spontaneous breathing; VC, controlled breathing (ventilator); VCCO2, controlled breathing with CO2 stimulation; VCR, controlled breathing after removal of CO2 stimulation. Bars depict mean values, with indication of 1 standard deviation.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4664703&req=5

Figure 3: Amplitude of the N2-P2 component of laser-evoked potentials (12 subjects). FB, free spontaneous breathing; VC, controlled breathing (ventilator); VCCO2, controlled breathing with CO2 stimulation; VCR, controlled breathing after removal of CO2 stimulation. Bars depict mean values, with indication of 1 standard deviation.
Mentions: The pain evaluated by the subjects at the laser perception threshold was 25 ± 13% of full scale on the pain VAS. Table 2 summarizes the LEPs amplitudes and latencies for all experimental conditions. A statistically significant attenuation of N2-P2 amplitude was observed during VC compared to FB (Δ = 24.0% ± 21.1%, p < 0.05, effect-size = 0.74) (Figures 3, 4). Further attenuation occurred during the VCCO2 condition (VC vs. VCCO2: Δ = 22.6% ± 17.9%, p < 0.05, effect-size = 0.53) (Figures 3, 4). Of note, the VC-associated reduction in N2-P2 was driven by reduction in P2 without significant change in N2, while the VCCO2-associated further reduction in N2-P2 was driven by a reduction in N2 without significant change in P2. We observed a trend to recovery between the VCCO2 and VCR conditions but not significant (VCCO2 vs. VCR: Δ = 32% ± 53%, ns effect-size = 0.36).

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Sorbonne Universités, University Pierre et Marie Curie Univ Paris 06, UMR_S 1158 "Neurophysiologie Respiratoire Expérimentale et Clinique" Paris, France ; Institut National de la Santé et de la Recherche Médicale, UMR_S 1158 "Neurophysiologie Respiratoire Expérimentale et Clinique" Paris, France ; Assistance Publique des Hôpitaux de Paris, Groupe Hospitalier Pitié-Salpêtrière Charles Foix, Service de Pneumologie et Réanimation Médicale (Département "R3S") Paris, France.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus