Dyspnea as a Noxious Sensation: Inspiratory Threshold Loading May Trigger Diffuse Noxious Inhibitory Controls in Humans

• Published in: Journal of neurophysiology 2007-02, Vol.97 (2), p.1396-1404
• Main Authors: Morelot-Panzini, Capucine, Demoule, Alexandre, Straus, Christian, Zelter, Marc, Derenne, Jean-Philippe, Willer, Jean-Claude, Similowski, Thomas
• Format: Article
• Language: English
• Subjects: Adult; Animal biology; Dyspnea; Dyspnea - physiopathology; Electric Stimulation; H-Reflex; H-Reflex - physiology; Humans; Life Sciences; Male; Neural Pathways; Neural Pathways - physiopathology; Nociceptors; Nociceptors - physiology; Pain; Pain - physiopathology; Peripheral Nervous System; Peripheral Nervous System - physiopathology; Phrenic Nerve; Phrenic Nerve - physiology; Reflex; Reflex - physiology; Respiratory Mechanics; Respiratory Mechanics - physiology; Veterinary medicine and animal Health
• ISSN: 0022-3077; 1522-1598
• DOI: 10.1152/jn.00116.2006

1 Laboratoire de Physiopathologie Respiratoire, Service de Pneumologie, 2 Service Central d'Explorations Fonctionnelles Respiratoires, and 3 Fédération de Neurophysiologie Clinique and Institut National de la Santé et de la Recherche Médicale U731, Assistance Publique— Hôpitaux de Paris, Groupe Hospitalier Pitié Salpétrière; and 4 Université Paris 6, Unité Propae de Recherche de l'Énseignement Superior EA 2397, Paris, France Submitted 2 February 2006; accepted in final form 20 July 2006 Dyspnea, a leading respiratory symptom, shares many clinical, physiological, and psychological features with pain. Both activate similar brain areas. The neural mechanisms of dyspnea are less well described than those of pain. The present research tested the hypothesis of common pathways between the two sensations. Six healthy men (age 30–40 yr) were studied. The spinal nociceptive flexion reflex (RIII) was first established in response to electrical sural stimulation. Dyspnea was then induced through inspiratory threshold loading, forcing the subjects to develop 70% of their maximal inspiratory pressure to inhale. This led to progressive inhibition of the RIII reflex that reached 50 ± 12% during the fifth minute of loading ( P < 0.001), was correlated to the intensity of the self-evaluated respiratory discomfort, and had recovered 5 min after removal of the load. The myotatic H-reflex was not inhibited by inspiratory loading, arguing against postsynaptic alpha motoneuron inhibition. Dyspnea, like pain, thus induced counterirritation, possibly indicating a C-fiber stimulation and activation of diffuse noxious inhibitory descending controls known to project onto spinal dorsal horn wide dynamic range neurons. This confirms the noxious nature of certain types of breathlessness, thus opening new physiological and perhaps therapeutic perspectives. Address for reprint requests and other correspondence: T. Similowski, Laboratoire de Physiopathologie Respiratoire, Service de Pneumologie et de Réanimation, Groupe Hospitalier Pitié Salpétrière, 47-83 boulevard de l'Hôpital, 75651 Paris Cedex 13, France (E-mail: thomas.similowski{at}psl.ap-hop-paris.fr )