Rapid-eye-movement-specific sleep-disordered breathing: A possible cause of excessive daytime sleepiness

Department of Medicine, Cooper Hospital/University Medical Center, Camden, NJ 08103, USA.
American Journal of Respiratory and Critical Care Medicine (Impact Factor: 13). 07/1996; 154(1):167-9. DOI: 10.1164/ajrccm.154.1.8680674
Source: PubMed


Some patients referred for polysomnography with complaints of excessive daytime sleepiness (EDS) and clinically suspected obstructive sleep apnea (OSA) have a respiratory disturbance index (RDI) < 10. Many would consider these patients not to have OSA. We reviewed 34 such patients to determine whether respiratory disturbances confined primarily to rapid eye movement (REM) sleep correlated with an objective criterion for EDS: a mean sleep latency (MSL) < 10 min. REM-specific events were quantified with indices calculated for REM sleep alone. Univariate linear regression showed that a REM-specific respiratory disturbance index (REM-RDI) and the transient arousal index (TAI) computed for REM sleep (REM-TAI) were associated with a low MSL (R2 = -0.35, p = 0.001; and R2 = -0.27, p = 0.01, respectively). In our subjectively sleepy patients with an overall RDI < 10, a REM-RDI > or = 15 had the highest predictive accuracy (82%) for an MSL < 10 min. Seventeen of the 34 study patients had a REM-RDI > or = 15. Their mean MSL was 8.3 +/- 0.8 min. We conclude that within a group of patients with daytime sleepiness, suspected OSA, and a normal RDI, there may be a subset who have clinically significant REM-specific sleep-disordered breathing.

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    • "It is important to note, that the neuromodulatory mechanisms contributing to OSA and CA are likely very different. The number of apneas significantly increases during REM sleep in OSA patients, and some patients show apneas exclusively during REM sleep (Eckert et al., 2009b; Findley et al., 1985; Kass et al., 1996). By contrast, the number of central apneas is lowest during REM sleep (Eckert et al., 2007a). "
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    ABSTRACT: Apnea, the cessation of breathing, is a common physiological and pathophysiological phenomenon with many basic scientific and clinical implications. Among the different forms of apnea, obstructive sleep apnea (OSA) is clinically the most prominent manifestation. OSA is characterized by repetitive airway occlusions that are typically associated with peripheral airway obstructions. However, it would be a gross oversimplification to conclude that OSA is caused by peripheral obstructions. OSA is the result of a dynamic interplay between chemo- and mechanosensory reflexes, neuromodulation, behavioral state and the differential activation of the central respiratory network and its motor outputs. This interplay has numerous neuronal and cardiovascular consequences that are initially adaptive but in the long-term become major contributors to the morbidity and mortality associated with OSA. However, not only OSA, but all forms of apnea have multiple, and partly overlapping mechanisms. In all cases the underlying mechanisms are neither "exclusively peripheral" nor "exclusively central" in origin. While the emphasis has long been on the role of peripheral reflex pathways in the case of OSA, and central mechanisms in the case of central apneas, we are learning that such a separation is inconsistent with the integration of these mechanisms in all cases of apneas. This review discusses the complex interplay of peripheral and central nervous components that characterizes the cessation of breathing.
    Respiratory Physiology & Neurobiology 06/2013; 189(2). DOI:10.1016/j.resp.2013.06.004 · 1.97 Impact Factor
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    • "Moreover, some sleep-related disorders are associated with REM sleep. REM sleep-dependent OSA (Kass et al 1996), nightmare and REM sleep behavior disorder (Schenck and Mahowald 1996) occur predominantly in REM sleep. For these reasons, estimation for the onset and duration of REM sleep is important not only for the scientific investigation, but also for the clinical evaluation of sleep-related disorders. "
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    ABSTRACT: Polysomnography (PSG) is currently considered the gold standard for assessing sleep quality. However, the numerous sensors that must be attached to the subject can disturb sleep and limit monitoring to within hospitals and sleep clinics. If data could be obtained without such constraints, sleep monitoring would be more convenient and could be extended to ordinary homes. During rapid-eye-movement (REM) sleep, respiration rate and variability are known to be greater than in other sleep stages. Hence, we calculated the average rate and variability of respiration in an epoch (30 s) by applying appropriate smoothing algorithms. Increased and irregular respiratory patterns during REM sleep were extracted using adaptive and linear thresholds. When both parameters simultaneously showed higher values than the thresholds, the epochs were assumed to belong to REM sleep. Thermocouples and piezoelectric-type belts were used to acquire respiratory signals. Thirteen healthy adults and nine obstructive sleep apnea (OSA) patients participated in this study. Kappa statistics showed a substantial agreement (kappa > 0.60) between the standard and respiration-based methods. One-way ANOVA analysis showed no significant difference between the techniques for total REM sleep. This approach can also be applied to the non-intrusive measurement of respiration signals, making it possible to automatically detect REM sleep without disturbing the subject.
    Physiological Measurement 10/2009; 30(12):1327-40. DOI:10.1088/0967-3334/30/12/003 · 1.81 Impact Factor
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    • "It is currently unclear whether or not REMS is decreased in clinical disorders with sleep fragmentation, as there are conflicting reports within and between disorders. For example, REMS has been reported to decrease (Kass et al., 1996; O'Connor et al., 2000) or remain unchanged in sleep apnea (Loadsman & Wilcox, 2000), and has been reported to increase to a greater extent in major depression than in post-traumatic stress disorder (Mellman et al., 1997). Although total NREMS time was unchanged in the SI rats, there was a reduction in the average duration of each individual sleep episode. "
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    ABSTRACT: Sleep fragmentation, a symptom in many clinical disorders, leads to cognitive impairments. To investigate the mechanisms by which sleep fragmentation results in memory impairments, rats were awakened once every 2 min via 30 s of slow movement on an automated treadmill. Within 1 h of this sleep interruption (SI) schedule, rats began to sleep in the 90-s periods without treadmill movement. Total non-rapid eye movement sleep (NREM) sleep time did not change over the 24 h of SI, although there was a significant decline in rapid eye movement sleep (REM) sleep and a corresponding increase in time spent awake. In the SI group, the mean duration of sleep episodes decreased and delta activity during periods of wake increased. Control rats either lived in the treadmill without movement (cage controls, CC), or had 10-min periods of movement followed by 30 min of non-movement allowing deep/continuous sleep (exercise controls, EC). EC did not differ from baseline in the total time spent in each vigilance state. Hippocampal long-term potentiation (LTP), a long-lasting change in synaptic efficacy thought to underlie declarative memory formation, was absent in rats exposed to 24 and 72 h SI. In contrast, LTP was normal in EC rats. However, long-term depression and paired-pulse facilitation were unaltered by 24 h SI. Twenty-four hour SI also impaired acquisition of spatial learning in the hippocampus-dependent water maze test. Twenty-four hour SI elevated plasma corticosterone (CORT) to levels previously shown to enhance LTP (125 ng/mL). The results suggest that sleep fragmentation negatively impacts spatial learning. Loss of N-methyl-D-aspartate (NMDA) receptor-dependent LTP in the hippocampal CA1 region may be one mechanism involved in this deficit.
    European Journal of Neuroscience 06/2006; 23(10):2739-48. DOI:10.1111/j.1460-9568.2006.04808.x · 3.18 Impact Factor
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