Dose-Dependent Effects of Transdermal Nicotine on Early Morning Awakening and Rapid Eye Movement Sleep Time in Nonsmoking Normal Volunteers

1994 ◽  
Vol 14 (4) ◽  
pp. 264???267 ◽  
Author(s):  
J. CHRISTIAN GILLIN ◽  
MICHAEL LARDON ◽  
CAROLINE RUIZ ◽  
SHAHROKH GOLSHAN ◽  
RAFAEL SALIN-PASCUAL
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):


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A300-A300
Author(s):  
L Zhang ◽  
J Zhu

Abstract Introduction Impaired rapid eye movement sleep is common among patients with Parkinson’s disease (PD). However, information on rapid eye movement density (REM density) among PD patients is currently lacking. The current study sought to characterize REM density in PD patients and to examine the associations between REM density sleep parameters and clinical manifestations. Methods We retrospectively recruited 172 PD patients. All participants were assessed with a two-night polysomnography, and REM density was calculated. Clinical assessments were completed in PD patients before polysomnography. Results Rapid eye movement sleep behavior disorder (RBD) were observed in 93 patients (54.1%). The disease duration, UPDRS part III score, Hoehn and Yahr (H-Y) stage, and HAMA, HAMD, and PDQ-39 scores in the Parkinson’s disease patients with rapid eye movement sleep behavior disorder (RBD) were significantly higher than in the patients without RBD (P<0.05). The REM density was also significantly higher in the RBD patients than in the patients without RBD (P<0.05). NREM sleep stage 3 time (N3 time) and percentage of N3 time of total sleep time (N3%) were higher in patients without RBD. The forward binary logistic regression model showed that REM density, UPDRS-III score and N3 sleep time were associated with RBD in the PD patients. Conclusion Our results confirm the high prevalence of RBD in patients with PD. Increased REM density was the main risk factor of RBD. Support Special Funds of the Jiangsu Provincial Key Research and Development Projects (grant No. BE2018610)


2019 ◽  
Vol 102 (6) ◽  
pp. 5458-5465 ◽  
Author(s):  
Emma Ternman ◽  
Emma Nilsson ◽  
Per Peetz Nielsen ◽  
Matti Pastell ◽  
Laura Hänninen ◽  
...  

1993 ◽  
Vol 74 (2) ◽  
pp. 545-548 ◽  
Author(s):  
T. Sato ◽  
M. Tadokoro ◽  
H. Kaba ◽  
H. Saito ◽  
K. Seto ◽  
...  

The presence of endogenous digitalis-like factors in the central nervous system suggests their functional significance in the central nervous system. Three-day infusions of three-stepped doses of the digitalis agent ouabain (1–100 ng.kg body wt-1.h-1) into the lateral cerebral ventricle of freely moving rats caused a dose-dependent increase in the number of central-apneic episodes during rapid-eye-movement sleep without affecting the time spent in rapid-eye-movement sleep or basic respiratory rate. These results suggest that endogenous digitalis-like factors may be involved in the genesis of central sleep apneas.


2012 ◽  
Vol 302 (12) ◽  
pp. R1411-R1425 ◽  
Author(s):  
S. Deurveilher ◽  
B. Rusak ◽  
K. Semba

To study sleep responses to chronic sleep restriction (CSR) and time-of-day influences on these responses, we developed a rat model of CSR that takes into account the polyphasic sleep patterns in rats. Adult male rats underwent cycles of 3 h of sleep deprivation (SD) and 1 h of sleep opportunity (SO) continuously for 4 days, beginning at the onset of the 12-h light phase (“3/1” protocol). Electroencephalogram (EEG) and electromyogram (EMG) recordings were made before, during, and after CSR. During CSR, total sleep time was reduced by ∼60% from baseline levels. Both rapid eye movement sleep (REMS) and non-rapid eye movement sleep (NREMS) during SO periods increased initially relative to baseline and remained elevated for the rest of the CSR period. In contrast, NREMS EEG delta power (a measure of sleep intensity) increased initially, but then declined gradually, in parallel with increases in high-frequency power in the NREMS EEG. The amplitude of daily rhythms in NREMS and REMS amounts was maintained during SO periods, whereas that of NREMS delta power was reduced. Compensatory responses during the 2-day post-CSR recovery period were either modest or negative and gated by time of day. NREMS, REMS, and EEG delta power lost during CSR were not recovered by the end of the second recovery day. Thus the “3/1” CSR protocol triggered both homeostatic responses (increased sleep amounts and intensity during SOs) and allostatic responses (gradual decline in sleep intensity during SOs and muted or negative post-CSR sleep recovery), and both responses were modulated by time of day.


2009 ◽  
Vol 110 (6) ◽  
pp. 1327-1334 ◽  
Author(s):  
Matthias Eikermann ◽  
Philipp Fassbender ◽  
Sebastian Zaremba ◽  
Amy S. Jordan ◽  
Carl Rosow ◽  
...  

Background Anesthetics depress both ventilatory and upper airway dilator muscle activity and thus put the upper airway at risk for collapse. However, these effects are agent-dependent and may involve upper airway and diaphragm muscles to varying degrees. The authors assessed the effects of pentobarbital on upper airway dilator and respiratory pump muscle function in rats and compared these results with the effects of normal sleep. Methods Tracheostomized rats were given increasing doses of pentobarbital to produce deep sedation then light and deep anesthesia, and negative pressure airway stimuli were applied (n = 11). To compare the effects of pentobarbital with those of natural sleep, the authors chronically instrumented rats (n = 10) with genioglossus and neck electromyogram and electroencephalogram electrodes and compared genioglossus activity during wakefulness, sleep (rapid eye movement and non-rapid eye movement), and pentobarbital anesthesia. Results Pentobarbital caused a dose-dependent decrease in ventilation and in phasic diaphragmatic electromyogram by 11 +/- 0.1%, but it increased phasic genioglossus electromyogram by 23 +/- 0.2%. Natural non-rapid eye movement sleep and pentobarbital anesthesia (10 mg/kg intraperitoneally) decreased respiratory genioglossus electromyogram by 61 +/- 29% and 45 +/- 35%, respectively, and natural rapid eye movement sleep caused the greatest decrease in phasic genioglossus electromyogram (95 +/- 0.3%). Conclusions Pentobarbital in rats impairs respiratory genioglossus activity compared to the awake state, but the decrease is no greater than seen during natural sleep. During anesthesia, in the absence of pharyngeal airflow, phasic genioglossus activity is increased in a dose-dependent fashion.


2019 ◽  
Vol 131 (2) ◽  
pp. 401-409 ◽  
Author(s):  
Lauren K. Dunn ◽  
Amanda M. Kleiman ◽  
Katherine T. Forkin ◽  
Allison J. Bechtel ◽  
Stephen R. Collins ◽  
...  

AbstractEditor’s PerspectiveWhat We Already Know about This TopicWhat This Article Tells Us That Is NewBackgroundResidency programs utilize night float systems to adhere to duty hour restrictions; however, the influence of night float on resident sleep has not been described. The study aim was to determine the influence of night float on resident sleep patterns and quality of sleep. We hypothesized that total sleep time decreases during night float, increases as residents acclimate to night shift work, and returns to baseline during recovery.MethodsThis was a single-center observational study of 30 anesthesia residents scheduled to complete six consecutive night float shifts. Electroencephalography sleep patterns were recorded during baseline (three nights), night float (six nights), and recovery (three nights) using the ZMachine Insight monitor (General Sleep Corporation, USA). Total sleep time; light, deep, and rapid eye movement sleep; sleep efficiency; latency to persistent sleep; and wake after sleep onset were observed.ResultsMean total sleep time ± SD was 5.9 ± 1.9 h (3.0 ± 1.2.1 h light; 1.4 ± 0.6 h deep; 1.6 ± 0.7 h rapid eye movement) at baseline. During night float, mean total sleep time was 4.5 ± 1.8 h (1.4-h decrease, 95% CI: 0.9 to 1.9, Cohen’s d = –1.1, P < 0.001) with decreases in light (2.2 ± 1.1 h, 0.7-h decrease, 95% CI: 0.4 to 1.1, d = –1.0, P < 0.001), deep (1.1 ± 0.7 h, 0.3-h decrease, 95% CI: 0.1 to 0.4, d = –0.5, P = 0.005), and rapid eye movement sleep (1.2 ± 0.6 h, 0.4-h decrease, 95% CI: 0.3 to 0.6, d = –0.9, P < 0.001). Mean total sleep time during recovery was 5.4 ± 2.2 h, which did not differ significantly from baseline; however, deep (1.0 ± 0.6 h, 0.4-h decrease, 95% CI: 0.2 to 0.6, d = –0.6, P = 0.001 *, P = 0.001) and rapid eye movement sleep (1.2 ± 0.8 h, 0.4-h decrease, 95% CI: 0.2 to 0.6, d = –0.9, P < 0.001 P < 0.001) were significantly decreased.ConclusionsElectroencephalography monitoring demonstrates that sleep quantity is decreased during six consecutive night float shifts. A 3-day period of recovery is insufficient for restorative sleep (rapid eye movement and deep sleep) levels to return to baseline.


CHEST Journal ◽  
2009 ◽  
Vol 136 (4) ◽  
pp. 67S
Author(s):  
Zinobia Khan ◽  
Moses Bachan ◽  
Sara Hyatt ◽  
Joseph Ghassibi ◽  
Stephen Lund ◽  
...  

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