scholarly journals Natural History of Sleep-disordered Breathing during Rapid Eye Movement Sleep. Relevance for Incident Cardiovascular Disease

2020 ◽  
Vol 17 (5) ◽  
pp. 614-620 ◽  
Author(s):  
R. Nisha Aurora ◽  
Elizabeth J. McGuffey ◽  
Naresh M. Punjabi
2009 ◽  
Vol 45 (7) ◽  
pp. 330-334 ◽  
Author(s):  
Francisco Campos-Rodríguez ◽  
Ana Fernández-Palacín ◽  
Nuria Reyes-Núñez ◽  
Ángela Reina-González

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A324-A324
Author(s):  
Tuyet Pham ◽  
Sonal Malhotra

Abstract Introduction Parasomnias are abnormal sleep-related movements that can occur during non-rapid eye movement sleep, rapid eye movement sleep, or transition of sleep. The prevalence of parasomnias in young children ranges from 9–40% which may be underestimated as this relies on parental recall. There are multiple reported cases of pharmacologically-induced parasomnias. Quetiapine is an atypical antipsychotic medication associated with somnambulism and sleep-related eating disorder. Report of case(s) A 9-year-old female with a history of attention deficit hyperactivity disorder, post-traumatic-stress disorder, depression, and sexual abuse during childhood presented to the Sleep Medicine Clinic for two years of worsened sleepwalking and sleep eating. Her medications included Methylphenidate, Quetiapine, Clonidine, and Duloxetine. She has had parasomnias since she was 3-years-old, initially presenting as abnormal sleeping positions (standing or sitting). She was initiated on Seroquel at 4-years-old, but parasomnias worsened over the last two years when Quetiapine was increased from 50 mg to 200 mg for behavioral and mood issues. Her somnambulism began to occur nightly. The family was required to remove all items from her bedroom except for the bed to prevent major injuries. She also had significant changes to her eating habit: she would eat two to three times her normal quantity as well as eating while asleep. The family would find her eating ice cream, chips, grapes, cold tortillas, or anything she was able to access. Fortunately, she did not consume raw meat or other frozen foods. The child did not have any recollection of eating at night. Psychiatry worked with her to cross-taper Quetiapine and Topiramate. At the lower dose of Quetiapine, she had exacerbation of her mood symptoms, paranoia, and insomnia; therefore, Topiramate was discontinued and Quetiapine was titrated to 150 mg with improvement in mood symptoms, insomnia, and resolution of sleep-related eating disorder. She continues to have somnambulism. Conclusion This case illustrates that quetiapine-induced somnambulism and sleep-related eating disorder can be dose-dependent; thus, important for clinicians to educate patients and/or family members of adverse effects while titrating quetiapine. Support (if any):


2001 ◽  
Vol 91 (6) ◽  
pp. 2758-2766 ◽  
Author(s):  
Y. Tagaito ◽  
V. Y. Polotsky ◽  
M. J. Campen ◽  
J. A. Wilson ◽  
A. Balbir ◽  
...  

To investigate the pathophysiological sequelae of sleep-disordered breathing (SDB), we have developed a mouse model in which hypoxia was induced during periods of sleep and was removed in response to arousal or wakefulness. An on-line sleep-wake detection system, based on the frequency and amplitude of electroencephalograph and electromyograph recordings, served to trigger intermittent hypoxia during periods of sleep. In adult male C57BL/6J mice ( n= 5), the sleep-wake detection system accurately assessed wakefulness (97.2 ± 1.1%), non-rapid eye movement (NREM) sleep (96.0 ± 0.9%) and rapid eye movement (REM) sleep (85.6 ± 5.0%). After 5 consecutive days of SDB, 554 ± 29 (SE) hypoxic events were recorded over a 24-h period at a rate of 63.6 ± 2.6 events/h of sleep and with a duration of 28.2 ± 0.7 s. The mean nadir of fraction of inspired O2 (Fi O2 ) on day 5 was 13.2 ± 0.1%, and 137.1 ± 13.2 of the events had a nadir Fi O2 <10% O2. Arterial blood gases confirmed that hypoxia of this magnitude lead to a significant degree of hypoxemia. Furthermore, 5 days of SDB were associated with decreases in both NREM and REM sleep during the light phase compared with the 24-h postintervention period. We conclude that our murine model of SDB mimics the rate and magnitude of sleep-induced hypoxia, sleep fragmentation, and reduction in total sleep time found in patients with moderate to severe SDB in the clinical setting.


Circulation ◽  
2011 ◽  
Vol 123 (12) ◽  
pp. 1280-1286 ◽  
Author(s):  
Hassan A. Chami ◽  
Helaine E. Resnick ◽  
Stuart F. Quan ◽  
Daniel J. Gottlieb

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