Obstructive sleep apnea (OSA) is a growing sleep-related breathing disorder with a major clinical impact that ranges from sleep fragmentation to arterial hypertension, to diabetes and neurodegenerative ailments. The major OSA underlying mechanisms are anatomical deficiencies of the upper airway, sleep-related dysfunction of upper airway dilator muscle reflexes and sleep-related depression of pharyngeal muscle tone. Decades of research have led to a great advancement in understanding OSA pathophysiology. However, there is still incomplete understanding of neurological causes of OSA, e.g., neurochemical mechanisms of state-dependent depression of upper airway reflexes and the neuronal control of pharyngeal muscles. Diagnostic technologies and assessment of upper airway properties, both functional and anatomical, may help to advance understanding of OSA pathophysiology. The knowledge of these mechanisms may facilitate the development of pharmacological treatment of OSA, which would be an important addition to currently available main therapeutic approaches, the continuous positive airway pressure and electrical stimulation of hypoglossal nerve. Major neurotransmitters that have been implicated in state-dependent control of motoneurons innervating upper airway muscles are glutamate, GABA, glycine, serotonin, noradrenaline, and acetylcholine. However, there is no consensus regarding the contribution of these neurotransmitters in the control of upper airway motoneurons.
This Research Topic will synthesize current knowledge from experts in the field regarding all aspects of OSA pathophysiology including, but not limited to, deficiency in upper airway anatomy and its neuronal compensation during wakefulness, sleep-related depression of upper airway reflexes, sleep-related impairment of excitability of motoneurons that control pharyngeal muscles, diagnostic modalities to identify upper airway dysfunction and upper airway morphology, development of animal models of OSA, and advances in OSA treatment.
We believe that this Research Topic will be of great value for researchers who are interested in OSA pathophysiology, as well as attract new generation of researchers to this important field. We welcome the following manuscript types to be submitted: reviews, mini-reviews, commentaries, original research reports, theoretical and computational studies, and methodological articles.
Obstructive sleep apnea (OSA) is a growing sleep-related breathing disorder with a major clinical impact that ranges from sleep fragmentation to arterial hypertension, to diabetes and neurodegenerative ailments. The major OSA underlying mechanisms are anatomical deficiencies of the upper airway, sleep-related dysfunction of upper airway dilator muscle reflexes and sleep-related depression of pharyngeal muscle tone. Decades of research have led to a great advancement in understanding OSA pathophysiology. However, there is still incomplete understanding of neurological causes of OSA, e.g., neurochemical mechanisms of state-dependent depression of upper airway reflexes and the neuronal control of pharyngeal muscles. Diagnostic technologies and assessment of upper airway properties, both functional and anatomical, may help to advance understanding of OSA pathophysiology. The knowledge of these mechanisms may facilitate the development of pharmacological treatment of OSA, which would be an important addition to currently available main therapeutic approaches, the continuous positive airway pressure and electrical stimulation of hypoglossal nerve. Major neurotransmitters that have been implicated in state-dependent control of motoneurons innervating upper airway muscles are glutamate, GABA, glycine, serotonin, noradrenaline, and acetylcholine. However, there is no consensus regarding the contribution of these neurotransmitters in the control of upper airway motoneurons.
This Research Topic will synthesize current knowledge from experts in the field regarding all aspects of OSA pathophysiology including, but not limited to, deficiency in upper airway anatomy and its neuronal compensation during wakefulness, sleep-related depression of upper airway reflexes, sleep-related impairment of excitability of motoneurons that control pharyngeal muscles, diagnostic modalities to identify upper airway dysfunction and upper airway morphology, development of animal models of OSA, and advances in OSA treatment.
We believe that this Research Topic will be of great value for researchers who are interested in OSA pathophysiology, as well as attract new generation of researchers to this important field. We welcome the following manuscript types to be submitted: reviews, mini-reviews, commentaries, original research reports, theoretical and computational studies, and methodological articles.
