[Central sleep apnea syndrome and Cheyne-Stokes respiration]. / Zentrales Schlafapnoe Syndrom und periodische Atmung.

This overview discusses pathogenesis, clinical presentation, prognostic implications and therapy of central sleep apnea with special reference to Cheyne-Stokes-Respiration or periodic breathing. In contrast to obstructive sleep apnea due to upper airway collapse during sleep, central sleep apnea (CSA) is mainly due to an instability of the breathing control system. Causes of central sleep apnea include alveolar hypoventilation disorders, heart failure, neurologic and autonomic disorders and idiopathic forms of CSA. Patients with idiopathic CSA often complain of insomnia and awakening during sleep but may also suffer from daytime sleepiness. Cheyne-Stokes-Respiration or peridic breathing is often associated with heart failure and neurological disorders especially those involving the brainstem. In heart failure periodic breathing has enormous prognostic implications. Treatment options for central sleep apnea are oxygen supplementation, medical therapy (i.e. acetazolamide) and CPAP. For patients with central sleep apnoea associated with alveolar hypoventilation nasal ventilation is treatment of choice. Newer nasal ventilation techniques (BiPAP, AutoSetCS) are under investigation for heart failure patients with Cheyne-Stokes-Respiration.

Laminar profiles of N-methyl-D-aspartate- and quisqualate-induced [Na+]o changes in rat hippocampus.

Since plastic changes in neuronal tissue are often associated with changes in responses to excitatory amino acids (EAA), a method is required which permits mapping of functional EAA receptor sites. In this study the measurement of extracellular sodium concentration changes [( Na+]o) induced by iontophoretic application of N-methyl-D-aspartate (NMDA) and quisqualate (Quis) is used as a tool to estimate the density of functional NMDA- and Quis-receptor sites in area CA1 and dentate gyrus of rat hippocampus. Largest decreases of [Na+]o induced by NMDA were found in basal and apical dendritic fields of area CA1 and in stratum moleculare of dentate gyrus at a distance of 50-100 microns from stratum granulare. Peak decreases in [Na+]o induced by Quis occurred at similar positions. Bath application of tetrodotoxin (TTX) suppressed that part of the extracellular Na+ loss mediated by Na+ fluxes through voltage activated Na+ channels. However, the laminar profiles of Quis- and NMDA-induced [Na+]o changes were not affected by TTX. Thus, EAA induced decreases in [Na+]o can be used to detect changes in receptor density and in receptor functionality of hippocampus which had undergone plastic changes.