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In 1973, the authors reported what seemed to be an unusual syndrome of sleep disturbance secondary to central apneas unrelated to any known disease. It was seen in snorers. Each respiratory event was associated with hypoxemia and increased pulmonary artery pressure. They went on to further investigate the impact of this syndrome on sleep and daytime behavior. Their current focus of interest is pharyngeal behavior during central sleep apneas, by monitoring electrical muscular activity of the pharynx, video imaging of the pharynx, and measurement of esophageal pressure. It took the authors several years to acquire five subjects for this study, partly because the disorder is uncommon and partly because some subjects refused to participate. Subjects were required to have at least 70% of respiratory events represented by central apneas. They underwent three nights of polysomnography to confirm the diagnosis. Then on the fourth day an otolaryngologist performed endocscopy of the upper airway to measure distances betweeen internal structures of the pharynx, followed by cephalometric X-rays to measure bone structures. That night, the endoscope was inserted in the nasopharynx all night, without any other recordings, while the subject's body position was maintained by an inflatable frame.Sleep and waking were judged behaviorally by inspection. The following day, a fiberoptic scope was placed through the nose and wire electrodes were hooked into the muscles of the upper airway. For that night, the fiberoptic scope was replaced, the electrodes remained, and the subject slept again in the molded shell. (From the article's description of the procedure, it seems understandable that some prospective subjects would have declined to participate!) The following night, an esophageal pressure monitor was substituted for the fiberoptic scope. Respiratory events that were analyzed had to occur during well-established sleep (stage 2 NREM), had to last at least 20 secs, and had to occur in the absence of chest or diaphragmatic muscle activity, esophageal pressure changes, and airflow. Such events were commonplace. The events analyzed also had to follow at least three normal, complete breaths and be at least two breaths removed from any arousal-associated hyperventilation or prior abnormal breathing. In each sequence of normal followed by abnormal breaths, the cross-sectional area of the airway was measured and that of normal breaths was assigned a value of 100% for comparison with airway area during abnormal breaths. Subjects were all male, ranging in age from 37 to 68 yrs, in BMI from 25 to 26, in RDI from 37 to 55, in proportion of central events from 78% to 98%, in proportion of mixed events from 2% to 22%. None had any purely obstructive events. The average duration of the central apneas was 26 secs. In all cases, the airway size decreased throughout its length during the apneic breaths, though there was never complete collapse. For the group as a whole, the mean maximal reduction in airway size was 71% (SD=4-8%), this maximum always occurring during the final two-thirds of the apnea. There was complete absence of muscular activity in the chest and diaphragm at the start of the apneas. This was associated with an absence of negative esophageal pressures. There was also complete absence or significant reduction in muscular activity of the pharynx and tongue. This finding indicated an absence of breathing effort. The apnea general terminated with an arousal associated with return of muscular activity and noisy breathing, even snoring. The authors acknowledged technical difficulties with their recording procedures. One difficulty was maintaining the subject's head and the endoscope in position, requiring the chin to be maintained in position. The equipment used impacted sleep, especially on the night with the fiberoptic scope which had the least total sleep time (about 4 1/2 hours). Central sleep apneas seem to involve a narrowing of the upper airway without any negative intrathoracic pressure or muscular activity in the upper airway, suggesting that the narrowing is a passive collapse. The effort to breathe in against a partially closed airway may trigger an arousal. However, they did not measure all possible pharyngeal muscles and it is possible that these became active during central apneas, though the authors found this doubtful. They regretted not having monitored blood carbon dioxide, which has been implicated by others in the cause of central sleep apnea, but doubted that a 20-second sleep apnea could be associated with significant change of blood carbon dioxide. they were impressed by the anatomical features of their central sleep apneics: with steep mandibular planes, high narrow hard palates, bite malocclusions, and low hyoid bones--features also associated with upper airway resistance syndrome, and perhaps influencing airway collapse. They noted, however, that their agreement with other researchers on a clear relationship between central and obstructive apneas, as exemplified by the response to nasal CPAP.

I fear that my summary cannot adequately convey the complexity (and seeming uncomfortableness) of the devices the authors used, especially to visualize the upper airway during sleep. Furthermore, the device used to maintain posture sounds rather like a restraint device that would add discomfort and severely limit postural changes and movements normal to sleep. When one compares results from such a study to comparative results with anesthetized rats as a model, the human subjects are clearly preferable, but the further the laboratory situation departs from normal sleep, the less convinced I feel that we are observing what actually happens in "normal" or at least "usual" sleep. If the authors had been less ambitious in obtaining such a large array of measures from each subject, they might have been able to more quickly secure a larger number of subjects, and prove different points separately with different groups. Five subjects--all too common a number in clinical sleep research--is really inadequate to take in the range of possible variation. For example, complete occlusion of the airway in sleep apnea could occur in quite a sizable minority of central sleep apneics and still be missed by accident in a random group of 5. I had some difficulty in reconciling the results described in this study with those of Xie and associates (Effects of inhaled CO2 and added dead space on idiopathic central sleep apnea) reviewed elsewhere on this website. The latter study described central apneas as typically posthyperventilatory, whereas the current authors appeared to deliberately eliminate posthyperventilatory phenomena from their definition of central apneas, without noting any frequent occurrence of such a pattern that was being ignored. One is left with the impression of the two research groups studying two different types of patients with two different types of central sleep apneas, but I doubt that is the case. More likely, the absence of blood CO2 monitoring left the present authors unaware of hyperventilatory episodes. It may be, from the wording of their methodology, that hyperventilations not associated with arousals, or occurring more than two breaths prior to the apnea, were being ignored. Nevertheless, one must respect the expertise and authority of the present research group too much to assume the occurrence of obvious errors. Their findings have not led me to abandon the impression that central apneas, in contrast to obstructive apneas, have something to do with blood CO2 levels and/or chemoreceptor sensitivity to those. But they do help convince me of some common underlying anatomical pathology in both central and obstructive sleep apneas--and upper airway resistance syndrome. It does, however, seem premature to say that all types of apnea are fundamentally anatomical in nature, and I doubt that the authors themselves would go so far.

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