PubMed · 5473750
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E P Grandjean. Fatigue.. https://doi.org/10.1080/0002889708506267
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This is an overview for the non-specialist of the pathophysiology, workup and treatment of the obstructive sleep apnea syndrome. The mechanisms leading to upper airway closure during sleep are discussed, as well as the current theoretical and experimental concepts for the apnea-induced arousal response and the consequent changes in sleep architecture and quality. Epidemiological data are summarized, with special reference to the problems of non-uniform definition criteria and examination techniques applied. In conclusion, a practical workup strategy and the current treatment options are summarized.
Seven infants with chronic neonatal lung disease and baseline oxygen saturation greater than 90% were studied with overnight polysomnography in their prescribed oxygen environment, and on a second night with 0.25 L/min additional oxygen. All had sleep fragmentation and decreased rapid-eye-movement (REM) sleep, which was reversed after the increased oxygen. Sleep duration (p < 0.003), percentage REM sleep (p < 0.001), and mean REM sleep period length (p < 0.001) were increased, and arousals in REM sleep decreased (p < 0.05), with improved oxygenation. We conclude that, in infants with chronic neonatal lung disease, arousal mechanisms minimise oxygen desaturation but induce sleep disruption.
Structural change in the hippocampal formation has become popular as a proposed neurobiological substrate for schizophrenic disorders. It is postulated that behavioral plasticity in the form of long-term potentiation of hippocampal synaptic transmission is an attractive putative mechanism for the mediation of transient psychosis. Moreover, the disturbed hippocampal neuroarchitecture found in schizophrenic brain may be susceptible to potentiation and dysfunctional to the degree that delusions and hallucinations develop. Partial and selective blockade of the receptors mediating potentiation may prove to be an efficient means of preventing psychotic episodes and avoiding further damage to the involved network. Basic research, utilizing experimental models such as intraventricular kainic acid injection, may help to clarify the anatomical and physiological substrate of psychosis.