Is brain damage really involved in the pathogenesis of obstructive sleep apnea?

Obstructive sleep apnea (OSA) syndrome is a surprisingly complex and highly individualized disease, with different factors contributing toward the disease process. Many factors can induce OSA disease, such as hypertrophy uvula, adenoidectomy, tonsil caused by mechanical obstruction of the airway, airway obstruction on obesity cause of decubitus, etc.; in addition, abnormal structure and function of the central nervous system (CNS) is also one of the important factors. This paper examines the relationship of the CNS with the onset of OSA. Evidence has shown that dysfunction of the CNS may be related to the occurrence of OSA. Although modification of the behaviors of the motor neurons may offer a potentially interesting means of controlling the airway, human afferent and motor pathways that regulate eupnea are still poorly understood. Combining some clinical phenomena of patients with cerebral hemorrhage or brain trauma at the temporal lobe, it seems that no close relation with OSA has been observed in clinical work and animal experiments; however, CNS damage at the temporal lobe is involved in the pathogenesis of OSA. This article examines the role of the CNS in the pathogenesis of OSA and its mechanisms. We have summarized previous findings of OSA-related brain damage, which were obtained by brain functional MRI, clinical, and animal experiment data to better understand the roles of the CNS in the pathogenesis of OSA. More specifically, this review summarizes how altered activity of the limbic system and its related structures could be associated with the occurrence of OSA. This conclusion may contribute toward our understanding of nosogenesis and the treatment of OSA.