Claire Launois1, Valérie Attali1,2,3, Marjolaine Georges1, Mathieu Raux1,2,4, Elise Morawiec1,2,5, Isabelle Rivals1,6, Isabelle Arnulf1,2,3, Thomas Similowski1,2,5. 1. Sorbonne Universités, UPMC Univ Paris 06, UMR_S 1158 "Neurophysiologie Respiratoire Expérimentale et Clinique", Paris, France. 2. INSERM, UMR_S 1158 "Neurophysiologie Respiratoire Expérimentale et Clinique", Paris, France. 3. AP-HP, Groupe Hospitalier Pitié-Salpêtrière Charles Foix, Service des Pathologies du Sommeil (Département "R3S"), Paris, France. 4. AP-HP, Groupe Hospitalier Pitié-Salpêtrière Charles Foix, Service de Surveillance Post-Interventionnelle et d'Accueil des Polytraumatisés (Département d'Anesthésie Réanimation), Paris, France. 5. AP-HP, Groupe Hospitalier Pitié-Salpêtrière Charles Foix, Service de Pneumologie et Réanimation Médicale (Département "R3S"), Paris, France. 6. Ecole Supérieure de Physique et de Chimie de la Ville de Paris, Paris, France.
Abstract
STUDY OBJECTIVES: The obstructive sleep apnea syndrome (OSAS) involves recurrent sleep-related upper airways (UA) collapse. UA mechanical properties and neural control are altered, imposing a mechanical load on inspiration. UA collapse does not occur during wakefulness, hence arousal-dependent compensation. Experimental inspiratory loading in normal subjects elicits respiratory-related cortical activity. The objective of this study was to test whether awake OSAS patients would exhibit a similar cortical activity. DESIGN: Descriptive physiology study. SETTING: Sleep laboratory in a large university affiliated tertiary hospital. PATIENTS: 26 patients with moderate OSAS according to polysomnography (5 < apnea-hypopnea index [AHI] ≤ 30, n = 14) or severe OSAS (AHI > 30, n = 12); 13 non-OSAS patients for comparison. INTERVENTIONS: None. MEASUREMENTS: Respiratory time-locked electroencephalographic segments ensemble averaged and analyzed for slow premotor potentials preceding inspiration ("pre-inspiratory potentials" [PIPs]). RESULTS: PIPs were present in 1/13 controls and 11/26 patients (P = 0.0336; 4/14 "moderate" and 7/12 "severe" patients). Awake OSAS patients therefore exhibit respiratory-related cortical activity during quiet breathing significantly more frequently than non-OSAS individuals. The corresponding PIPs resemble those observed during prepared voluntary inspirations and in response to experimental inspiratory loads in normal subjects, which involve a cortical network comprising the supplementary motor area. CONCLUSIONS: A respiratory-related cortical activity could contribute to the increased neural drive to upper airway and to inspiratory muscles that has previously been described in obstructive sleep apnea, and could therefore contribute to the arousal-dependent compensation of upper airway abnormalities. Whether or not such cortical compensatory mechanisms have cognitive consequences remains to be determined.
STUDY OBJECTIVES: The obstructive sleep apnea syndrome (OSAS) involves recurrent sleep-related upper airways (UA) collapse. UA mechanical properties and neural control are altered, imposing a mechanical load on inspiration. UA collapse does not occur during wakefulness, hence arousal-dependent compensation. Experimental inspiratory loading in normal subjects elicits respiratory-related cortical activity. The objective of this study was to test whether awake OSAS patients would exhibit a similar cortical activity. DESIGN: Descriptive physiology study. SETTING: Sleep laboratory in a large university affiliated tertiary hospital. PATIENTS: 26 patients with moderate OSAS according to polysomnography (5 < apnea-hypopnea index [AHI] ≤ 30, n = 14) or severe OSAS (AHI > 30, n = 12); 13 non-OSAS patients for comparison. INTERVENTIONS: None. MEASUREMENTS: Respiratory time-locked electroencephalographic segments ensemble averaged and analyzed for slow premotor potentials preceding inspiration ("pre-inspiratory potentials" [PIPs]). RESULTS:PIPs were present in 1/13 controls and 11/26 patients (P = 0.0336; 4/14 "moderate" and 7/12 "severe" patients). Awake OSAS patients therefore exhibit respiratory-related cortical activity during quiet breathing significantly more frequently than non-OSAS individuals. The corresponding PIPs resemble those observed during prepared voluntary inspirations and in response to experimental inspiratory loads in normal subjects, which involve a cortical network comprising the supplementary motor area. CONCLUSIONS: A respiratory-related cortical activity could contribute to the increased neural drive to upper airway and to inspiratory muscles that has previously been described in obstructive sleep apnea, and could therefore contribute to the arousal-dependent compensation of upper airway abnormalities. Whether or not such cortical compensatory mechanisms have cognitive consequences remains to be determined.
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