We tested the hypotheses that active upper airway closure during induced central apneas in nonsedated lambs 1). is complete and occurs at the laryngeal level and 2). is not due to stimulation of the superior laryngeal nerves (SLN). Five newborn lambs were surgically instrumented to record thyroarytenoid (TA) muscle (glottal constrictor) electromyographic (EMG) activity with supra- and subglottal pressures. Hypocapnic and nonhypocapnic central apneas were induced before and after SLN sectioning in the five lambs. A total of 174 apneas were induced, 116 before and 58 after sectioning of the internal branch of the SLN (iSLN). Continuous TA EMG activity was observed in 88% of apneas before iSLN section and in 87% of apneas after iSLN section. A transglottal pressure different from zero was observed in all apneas with TA EMG activity, with a mean subglottal pressure of 4.3 +/- 0.8 cmH2O before and 4.7 +/- 0.7 cmH2O after iSLN section. Supraglottal pressure was consistently atmospheric. Sectioning of both iSLNs had no effects on the results. We conclude that upper airway closure during induced central apneas in lambs is active, complete, and occurs at the glottal level only. Consequently, a positive subglottal pressure is maintained throughout the apnea. Finally, this complete active glottal closure is independent from laryngeal afferent innervation.
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http://dx.doi.org/10.1152/japplphysiol.00773.2002 | DOI Listing |
Sleep Med
January 2025
CHU Angers, Department of Respiratory and Sleep Medicine, F-49933, Angers, France; Univ Angers, Faculty of Medicine, F-49000 Angers, France.
Objectives: Treatment-emergent central sleep apnea (TECSA) is well established in continuous positive airway pressure therapy but was barely studied in mandibular advancement device (MAD) treatment. This study aims to evaluate the prevalence of TECSA in patients treated with a MAD and to determine its risk factors and clinical relevance.
Materials And Methods: A total of 139 patients from the IRSR Pays de la Loire Sleep Cohort suffering from snores or obstructive sleep apnea syndrome (OSAS) and treated with a custom-made titratable MAD were included.
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November 2024
Division of Neonatology, Department of Women's and Children's Health, University of Leipzig Medical Center, Liebigstraße 20a, 04103, Leipzig, Germany.
Purpose: Ureaplasma species (spp.) are relevant contributors to preterm birth but may also cause invasive infections particularly in very immature preterm infants. This study aimed to assess the incidence of neonatal Ureaplasma infections of the central nervous system (CNS).
View Article and Find Full Text PDFTher Adv Respir Dis
January 2025
Division of Pulmonary and Sleep Medicine, Department of Pediatrics, University of Washington School of Medicine, Seattle Children's Hospital, 4800 Sand Point Way NE, OC 7.730, Seattle, WA 98105, USA.
Background: Joubert syndrome (JS) is an autosomal recessive disorder with a distinctive mid-hindbrain malformation known as the "molar tooth sign" which involves the breathing control center and its connections with other structures. Literature has reported significant respiratory abnormalities which included hyperpnea interspersed with apneic episodes during wakefulness. Larger-scale studies looking at polysomnographic findings or subjective reports of sleep problems in this population have not yet been published.
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January 2025
Division of Orthogenetics, Department of Pediatrics, Nemours Children's Hospital, Delaware, 1600 Rockland Road, Wilmington, DE, 19803, USA.
Achondroplasia is the most common disproportionate short-stature skeletal dysplasia. Features associated with achondroplasia are rhizomelia, macrocephaly, midface hypoplasia, and typical cognition. Potential medical complications include foramen magnum stenosis, hydrocephalus, middle ear dysfunction, obstructive and central sleep apnea, spinal stenosis and genu varum.
View Article and Find Full Text PDFRespir Res
January 2025
Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Background: Obstructive sleep apnea (OSA) is frequently associated with increased incidence and mortality of pulmonary hypertension (PH). The immune response contributes to pulmonary artery remodeling and OSA-related diseases. The immunologic factors linked to OSA-induced PH are not well understood.
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