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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.


Related in: MedlinePlus

Experimental set up used to induce experimental dyspnea. Dyspnea was induced by enriching the inspired gas in CO2 (i.e., increasing FiCO2) while hindering the ventilatory response to CO2 by controlling breathing with a ventilator (fixed tidal volume and respiratory rate, as determined during a preliminary training session to ensure passive ventilation of the subjects to be). FiCO2 was fine-tuned in order to maintain respiratory discomfort between 5 and 6 on a 10 cm “respiratory discomfort” visual analog scale (VAS). Flow, mouth pressure, and PetCO2 were monitored continuously during the session.
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Figure 1: Experimental set up used to induce experimental dyspnea. Dyspnea was induced by enriching the inspired gas in CO2 (i.e., increasing FiCO2) while hindering the ventilatory response to CO2 by controlling breathing with a ventilator (fixed tidal volume and respiratory rate, as determined during a preliminary training session to ensure passive ventilation of the subjects to be). FiCO2 was fine-tuned in order to maintain respiratory discomfort between 5 and 6 on a 10 cm “respiratory discomfort” visual analog scale (VAS). Flow, mouth pressure, and PetCO2 were monitored continuously during the session.

Mentions: To induce air hunger, 95% CO2 was instilled into the inspiratory limb of the breathing circuit to increase the inspired fraction in CO2 (FiCO2) (Figure 1). The quantity of CO2 so administered was taylored on both PetCO2 (either maintained or increased, but never allowed to decrease) and on the degree of respiratory discomfort rated by the subjects that was maintained between 50 and 60% of the full dyspnea VAS scale. It ensues that the CO2 content of the inspired mixture varied between subjects and with time in a given subject.


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)

Experimental set up used to induce experimental dyspnea. Dyspnea was induced by enriching the inspired gas in CO2 (i.e., increasing FiCO2) while hindering the ventilatory response to CO2 by controlling breathing with a ventilator (fixed tidal volume and respiratory rate, as determined during a preliminary training session to ensure passive ventilation of the subjects to be). FiCO2 was fine-tuned in order to maintain respiratory discomfort between 5 and 6 on a 10 cm “respiratory discomfort” visual analog scale (VAS). Flow, mouth pressure, and PetCO2 were monitored continuously during the session.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4664703&req=5

Figure 1: Experimental set up used to induce experimental dyspnea. Dyspnea was induced by enriching the inspired gas in CO2 (i.e., increasing FiCO2) while hindering the ventilatory response to CO2 by controlling breathing with a ventilator (fixed tidal volume and respiratory rate, as determined during a preliminary training session to ensure passive ventilation of the subjects to be). FiCO2 was fine-tuned in order to maintain respiratory discomfort between 5 and 6 on a 10 cm “respiratory discomfort” visual analog scale (VAS). Flow, mouth pressure, and PetCO2 were monitored continuously during the session.
Mentions: To induce air hunger, 95% CO2 was instilled into the inspiratory limb of the breathing circuit to increase the inspired fraction in CO2 (FiCO2) (Figure 1). The quantity of CO2 so administered was taylored on both PetCO2 (either maintained or increased, but never allowed to decrease) and on the degree of respiratory discomfort rated by the subjects that was maintained between 50 and 60% of the full dyspnea VAS scale. It ensues that the CO2 content of the inspired mixture varied between subjects and with time in a given subject.

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