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Non-rapid Eye Movement (non-rapid + eye_movement)
Terms modified by Non-rapid Eye Movement Selected AbstractsAltered interaction between cardiac vagal influence and delta sleep EEG suggests an altered neuroplasticity in patients suffering from major depressive disorderACTA PSYCHIATRICA SCANDINAVICA, Issue 3 2010F. Jurysta Jurysta F, Kempenaers C, Lancini J, Lanquart J-P, van de Borne P, Linkowski P. Altered interaction between cardiac vagal influence and delta sleep EEG suggests an altered neuroplasticity in patients suffering from major depressive disorder. Objective:, Major depressive disorder (MDD), which is associated with altered neuroplasticity and increased relative cardiac sympathic activity, enhances the risk of cardiovascular pathologies. Interaction between cardiac sympatho-vagal indexes and delta sleep power is probably altered in MDD. Method:, Sleep characteristics and cardiac sympatho-vagal indexes of 10 depressive patients were compared to 10 control men across the first three non-rapid eye movement (NREM),REM cycles. Interaction between normalized high frequency (HF) and delta power bands was studied using coherence analysis. Results:, Patients showed increased sleep latency, stage 1 and wake durations. No differences in heart rate variabilities were observed: Total power, HF and RR-interval decreased from NREM to REM sleep and wakefulness in both groups. Gain value was lower in patients while coherence and phase shift were similar between groups. Modifications in HF appear 8 min before modifications in delta. Conclusion:, Major depressive disorder is related to an altered link between cardiac vagal influence and delta sleep, suggesting disorders in cardiovascular controls and an altered neuroplasticity. [source] Effects of Vigabatrin on Sleep,Wakefulness Cycle in Amygdala-Kindled RatsEPILEPSIA, Issue 2 2000Y. H. Raol Summary: Purpose: Our aim was to study the effect of prolonged administration of vigabatrin (VGB) on sleep-wakefulness cycle in kindled seizure-induced rats. Methods: Adult male Wistar rats were implanted stereotaxically with electrodes for kindling and polysomnography. The rats were divided into two groups, kindled and VGB-treated kindled rats. VGB was administered intraperitonially every day for 21 days, and polysomnographic recordings were taken after doses 1, 7, 14, and 21. The drug effects were evaluated by comparing the records of kindled and drug-treated kindled rats. Results: The VGB-administered kindled rats showed an increase in total sleep time (TST) due to an increase in total non-rapid eye movement (NREM) and light slow-wave sleep stage I (SI) with a decrease in wakefulness. The number of episodes and REM onset latencies were found to be decreased after drug treatment. Conclusions: It can therefore be concluded that VGB has a somnolence-inducing effect and that it might mediate its anti-convulsant effect by altering sleep architecture through sleep-regulating areas. [source] Sleep architecture in children with adenoidal hypertrophyJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 10 2006Xiao-Wen Zhang Aim: Adenoidal hypertrophy (AH) in children is associated with obstructive manifestations like mouth breathing, snoring. Unfortunately, little is known regarding sleep architecture of AH in children. The purpose of this study was therefore undertaken to investigate the polysomnographic variables in children with AH. Method: 47 children with AH and 11 controls underwent nocturnal polysomnography. Sleep was scored manually according to the standard set by Rechtschaffen. Results: In AH, stage 1 sleep percentage and rapid eye movement (REM) latency were increased significantly, while the sleep percentage of stage 2 and REM was decreased remarkably compared with that of controls. Arousal index in AH was much more higher than that in controls. Arousal index in REM sleep was higher than that in non-rapid eye movement (NREM) sleep in AH, but the number of arousals in REM sleep was lower than that in NREM sleep. Hypopnea events were the most common type of respiratory events, followed by obstructive events in AH and controls. Apnea/hypopnea index in AH was higher in comparison to controls. No significant difference was found between the children with AH and controls in SaO2 nadir (%) and base mean SaO2 (%). Apnea/hypopnea index was related to hypopnea arousal in REM sleep and hypoxemia arousal in NREM sleep. Conclusion: AH is predominantly characterised by a hypopnea with little obstruction in children. Our results clearly and for the first time demonstrated that sleep architecture was abnormal in children with AH. We therefore speculate that hypopnea arousal in REM sleep and hypoxemia arousal in NREM sleep may play an important role in the course of respiratory disturbance. [source] Role of Wake-Promoting Basal Forebrain and Adenosinergic Mechanisms in Sleep-Promoting Effects of EthanolALCOHOLISM, Issue 6 2010Mahesh M. Thakkar Background:, Ethanol intake has significant impact on sleep. However, the cellular substrates responsible for sleep promotion following ethanol intake are unknown. The purine nucleoside, adenosine, is responsible for mediating many neuronal and behavioral responses to ethanol. Studies performed in cell cultures suggest that ethanol inhibits equilibrative nucleoside transporter 1 to block the reuptake of adenosine resulting in increased extracellular adenosine. Adenosine also has a pivotal role in sleep regulation. Adenosine acts via A1 receptor to inhibit the wake-promoting neurons of the basal forebrain (BF) resulting in the promotion of sleep. Is ethanol-induced sleep associated with the inhibition of the BF wake-promoting neurons? Do adenosinergic mechanisms in the BF have a role in sleep-promoting effects of ethanol? Methods:, To address these questions, we performed 3 experiments in Sprague,Dawley rats. First, we verified the effect of ethanol on sleep promotion. Second, we evaluated the effect of ethanol on c-Fos expression (a marker of neuronal activation) in the BF wake-promoting neurons and third we monitored the effects of A1 receptor blockade in the BF on ethanol-induced sleep. Results:, Significant increase in non-rapid eye movement (NREM) sleep with a concomitant decrease in wakefulness was observed during the first 12 hours postethanol. REM sleep remained unaffected. Ethanol administration caused a significant decrease in the number of BF wake-promoting neurons with c-Fos immunoreactivity. Bilateral microinjections of a selective A1R receptor antagonist 8-cyclopentyl-1, 3-dipropylxanthine into the BF significantly attenuated sleep-promoting effects of ethanol. Conclusion:, These results suggest that the inhibition of BF wake-promoting neurons by adenosinergic mechanism may be responsible for the sleep promoting effects of ethanol. We believe our study is the first to investigate the cellular mechanisms responsible for the somnogenic effects of ethanol. [source] No persisting effect of partial sleep curtailment on cognitive performance and declarative memory recall in adolescentsJOURNAL OF SLEEP RESEARCH, Issue 1-Part-I 2010MARTA KOPASZ Summary Growing evidence indicates that sleep facilitates learning and memory processing. Sleep curtailment is increasingly common in adolescents. The aim of this study was to examine the effects of short-term sleep curtailment on declarative memory consolidation in adolescents. A randomized, cross-over study design was chosen. Twenty-two healthy subjects, aged 14,16 years, spent three consecutive nights in the sleep laboratory with a bedtime of 9 h during the first night (adaptation), 4 h during the second (partial sleep curtailment) and 9 h during the third night (recovery). The control condition consisted of three consecutive nights with bedtimes of 9 h. Both experimental conditions were separated by at least 3 weeks. The acquisition phase for the declarative tests was between 16:00 and 18:00 hours before the second night. Memory performance was examined in the morning after the recovery night. Executive function, attention and concentration were also assessed to control for any possible effects of tiredness. During the 4-h night, we observed a curtailment of 50% of non-rapid eye movement (non-REM), 5% of slow wave sleep (SWS) and 70% of REM sleep compared with the control night. Partial sleep curtailment of one night did not influence declarative memory retrieval significantly. Recall in the paired-associate word list task was correlated positively with percentage of non-REM sleep in the recovery night. Declarative memory consolidation does not appear to be influenced by short-term sleep curtailment in adolescents. This may be explained by the high ability of adolescents to compensate for acute sleep loss. The correlation between non-REM sleep and declarative memory performance supports earlier findings. [source] Differential effects of lorazepam on sleep and activity in C57BL/6J and BALB/cJ strain miceJOURNAL OF SLEEP RESEARCH, Issue 3 2009XIANGDONG TANG Summary Compared to C57BL/6 mice, BALB/c mice exhibit greater ,anxiousness' on behavioural tests of anxiety, and can show significantly longer sleep disruptions after exposure to anxiogenic situations. Relative to C57BL/6 mice, BALB/c mice also have reduced benzodiazepine (BZ) receptor densities in the brain and fivefold less BZ receptor density in the amygdala, a region important in anxiety and in the control of arousal. Lorazepam is a BZ receptor full agonist and has been used to treat both anxiety and insomnia. Differences between C57BL/6 and BALB/c mice raise the question of whether BZ agonists would impact sleep and activity differentially in the two strains. We examined the effects of two doses of lorazepam (0.5 and 1.5 mg kg,1) or saline alone (0.2 mL) on sleep and activity in C57BL/6 (n = 8) and BALB/c (n = 7) mice. Compared to saline, both doses of lorazepam significantly increased non-rapid eye movement (NREM) and reduced activity in both strains. In C57BL/6 mice, rapid eye movement (REM) was increased at both doses. In BALB/c mice, the 0.5 mg kg,1 dose had no significant influence on REM, whereas REM was reduced significantly after the 1.5 mg kg,1 dose. The results demonstrate significant differences between C57BL/6 and BALB/c mice in the effects of lorazepam on REM, whereas the effects on NREM and activity were similar. Strain differences in the number of BZ receptors in the amygdala, but not other brain regions, suggests possible site specificity in the effects of lorazepam on REM. These differences in BZ-binding sites in the amygdala could be a significant factor in differences in the sleep response between C57 and BALB/c mice. [source] Is the failure to detect stimulus deviance during sleep due to a rapid fading of sensory memory or a degradation of stimulus encoding?JOURNAL OF SLEEP RESEARCH, Issue 2 2005MERAV SABRI Summary The mismatch negativity (MMN) is thought to reflect the outcome of a system responsible for the detection of change in an otherwise repetitive, homogenous acoustic environment. This process depends on the storage and maintenance of a sensory representation of the frequently presented stimulus to which the deviant stimulus is compared. Few studies have been able to record the MMN in non-rapid eye movement (NREM) sleep. This pattern of results might be explained by either a rapid fading of sensory memory or an inhibition of stimulus input prior to entry into the cortical MMN generator site. The present study used a very rapid rate of presentation in an attempt to capture mismatch-related negativity prior to the fading of sensory memory. Auditory event-related potentials were recorded from 12 subjects during a single sleep period. A 1000 Hz standard stimulus was presented every 150 ms. At random, on 6.6% of the trials, the standard was changed to either a large 2000 Hz or a small 1100 Hz deviant. In wakefulness, the large deviant elicited an extended negativity that was reduced in amplitude following the presentation of the small deviant. This negativity was also apparent during REM sleep following the presentation of the large deviant. These deviant-related negativities (DRNs) were probably a composite of N1 and MMN activity. During NREM sleep (stage 2 and slow-wave sleep), only the large deviant continued to elicit a DRN. However this DRN might be overlapped by the initial activity of a component that is unique to sleep, the N350. There was little evidence of the DRN or the MMN during sleep following the presentation of the small deviant. A rapid rate of presentation, therefore, does not preserve the MMN following small deviance within sleep. It is possible that inhibition of sensory input occurs before entry into the MMN generating system in the temporal cortex. [source] Rapid tryptophan depletion reverses phenelzine-induced suppression of REM sleepJOURNAL OF SLEEP RESEARCH, Issue 1 2003Hans-Peter Landolt SUMMARY Treatment with the monoamine oxidase inhibitor phenelzine completely suppressed rapid eye movement (REM) sleep in five depressed patients. Hypothesizing that increased serotonergic neurotransmission eliminated REM sleep, we administered a tryptophan-free amino acid drink (TFD) known to reduce plasma tryptophan and brain levels of serotonin. The TFD reversed the REM sleep suppression, while the control drink (TFD plus tryptophan) had virtually no effect on sleep. Neither TFD nor control drink affected mood, total sleep time, sleep efficiency or the all-night electroencephalogram power spectra in non-rapid eye movement (NREM) sleep. We report the first non-disruptive, double-blind method for studying human subjects overnight with and without REM sleep. It opens up a novel strategy for investigating the functions of REM sleep, and the roles of serotonin and REM sleep in the regulation of NREM sleep and mood. [source] Time course of EEG background activity level before spontaneous awakening in infantsJOURNAL OF SLEEP RESEARCH, Issue 4 2002Chiara Zampi SUMMARY This research aimed to investigate the time course of the cortical activity level preceding spontaneous awakening as a function of age and state. Two groups of infants (1,4 and 9,14 weeks of age) were continuously monitored by polygraphic recording and behavioural observation during the night. The electroencephalographic (EEG) activity recorded by the C3,O1 lead was analysed through an automatic analysis method which provides, for each 30-s epoch, a single measure, time domain based, of the EEG synchronization. The EEG parameter values were computed in the 6 min preceding each awakening out of non-rapid eye movement (NREM) sleep and out of rapid eye movement (REM) sleep. The EEG background activity level did not change in the minutes preceding awakening out of REM sleep. Awakening out of NREM sleep was preceded by a change of EEG activity level in the direction of higher activation with different time course according to the age. Both REM and NREM sleep results suggest that a high level of EEG activity is a prerequisite for the occurrence of a spontaneous awakening. [source] Detection of gastric slow wave uncoupling from multi-channel electrogastrogram: validations and applicationsNEUROGASTROENTEROLOGY & MOTILITY, Issue 5 2003Z. S. Wang Abstract Current methodology of single channel electrogastrography is unable to detect coupling or uncoupling of gastric slow waves, which is crucial for gastric emptying. In this study, a new methodology, called cross-spectral analysis method, was established to compute the coupling percentage of multi-channel gastric slow waves recorded using serosal electrodes and electrogastrogram (EGG). Two experiments were performed to validate the method and demonstrate its applications in clinical research. In experiment 1, simultaneous recordings of gastric slow waves were made in five dogs from serosal electrodes and cutaneous electrodes. In experiment 2, four-channel fasting EGGs were made in 10 volunteers for 30 min during waking and 30 min during non-rapid eye movement (REM) sleep. The validation study (experiment 1) showed that the slow wave coupling calculated from the EGGs was correlated with that computed from the serosal recordings. The gastric slow wave coupling percentages detected from both serosal and cutaneous recordings were significantly impaired during vasopressin infusion (6.3 ± 2.6 vs 62.4 ± 6.3, P < 0.001 for serosal recordings; 6.7 ± 3.0 vs 57.2 ± 2.7, P < 0.001 for cutaneous recordings), and the coupling percentages respectively calculated from serosal and cutaneous recordings were significantly correlated during the baseline recording period (R = 0.922, P < 0.05) and vasopressin infusion period (R = 0.916, P < 0.05). In experiment 2, the gastric slow wave became less coupled when healthy volunteers fell asleep. The percentage of slow wave coupling calculated from the EGGs was 68.2 ± 17.9% during waking but 41.9 ± 20.8 during non-REM sleep (P < 0.05). The method developed in this study is reliable for the detection of slow wave uncoupling from multi-channel EGGs. Gastric slow wave coupling is impaired during vasopressin infusion and sleep. These data suggest that this method has potential applications in physiological and clinical studies. [source] Correlation between electroencephalography and heart rate variability during sleepPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 1 2003MMLSC , Mina Ako MT Abstract It is known that autonomic nervous activities change in correspondence with sleep stages. However, the characteristics of continuous fluctuations in nocturnal autonomic nerve tone have not been clarified in detail. The study aimed to determine the possible correlation between the electroencephalogram (EEG) and autonomic nervous activities, and to clarify in detail the nocturnal fluctuations in autonomic nerve activities. Overnight EEGs and electrocardiograms of seven healthy males were obtained. These EEGs were analyzed by fast Fourier transformation algorithm to extract delta, sigma and beta power. Heart rate and heart rate variability (HRV) were calculated in consecutive 5-min epochs. The HRV indices of low frequency (LF), high frequency (HF) and LF/HF ratio were calculated from the spectral analysis of R-R intervals. The sleep stages were manually scored according to Rechtschaffen and Kales' criteria. Low frequency and LF/HF were significantly lower during non-rapid eye movement (NREM) than REM, and were lower in stages 3 and 4 than in stages 1 and 2. Furthermore, delta EEG showed inverse correlations with LF (r = , 0.44, P < 0.001) and LF/HF (r = , 0.41, P < 0.001). In contrast, HF differed neither between REM and NREM nor among NREM sleep stages. Detailed analysis revealed that correlation was evident from the first to third NREM, but not in the fourth and fifth NREM. Delta EEG power showed negative correlations with LF and LF/HF, suggesting that sympathetic nervous activities continuously fluctuate in accordance with sleep deepening and lightening. [source] Treatment with leuprolide acetate decreases the threshold of the ventilatory response to carbon dioxide in healthy malesTHE JOURNAL OF PHYSIOLOGY, Issue 2 2004Jason H. Mateika This investigation was designed to determine if suppression of testosterone alters the ventilatory response to carbon dioxide in the presence of high and low levels of oxygen. Eleven healthy male subjects completed a series of rebreathing trials during wakefulness, before and after treatment with a long-acting gonadotropin-releasing hormone agonist. Five subjects also completed studies during non-rapid eye movement (NREM) sleep. During wakefulness, subjects initially hyperventilated to reduce the partial pressure of carbon dioxide (PET,CO2) below 25 Torr. Subjects then rebreathed from a bag containing a normocapnic (42 Torr), low (50 Torr) or high oxygen (140 Torr) gas mixture. During each trial PET,CO2 increased while oxygen was maintained at a constant level. The threshold of the ventilatory response to carbon dioxide was considered to be the point at which minute ventilation began to rise in a linear fashion as PET,CO2 increased. The slope of the ventilatory response above the threshold was used as a measure of sensitivity to carbon dioxide. During NREM sleep, hypocapnia was induced via nasal mechanical ventilation. Several trials were completed until the cessation of mechanical ventilation resulted in a central apnoea which demarcated the threshold of the ventilatory response to carbon dioxide. In response to treatment with leuprolide acetate, the threshold measured in wakefulness decreased during carbon dioxide rebreathing in the presence of low (41.05 ± 0.77 versus 39.40 ± 0.83 Torr; P= 0.01) and high (46.32 ± 0.56 versus 44.78 ± 0.83 Torr; P= 0.01) oxygen levels. An increase in sensitivity (4.82 ± 0.61 versus 7.17 ± 1.20 l min,1 Torr,1; P= 0.02) was also observed during rebreathing in the presence of high but not low oxygen levels. The increase in sensitivity was accompanied by an increase in carbon dioxide production. The findings observed during NREM sleep were similar to those observed during wakefulness, since the PET,CO2 that demarcated the threshold was decreased after leuprolide treatment (42.1 ± 0.6 versus 39.6 ± 0.6 Torr; P= 0.002). Additionally, the decrease in PET,CO2 required to induce an apnoea was greater after treatment with leuprolide (2.56 ± 0.25 versus 4.06 ± 0.29 Torr; P= 0.004). We conclude that suppression of testosterone decreases the threshold of the ventilatory response to carbon dioxide during both wakefulness and sleep. [source] CASE REPORTS: Abnormal Sexual Behavior During SleepTHE JOURNAL OF SEXUAL MEDICINE, Issue 12 2009Giacomo Della Marca MD ABSTRACT Introduction., Automatic, uncontrolled, and unaware sexual behaviors during sleep have occasionally been described. The clinical and polysomnographic features of nocturnal sexual behavior allow it to be considered a distinct parasomnia named "sexsomnia". Recently, abnormal sexual behaviors during sleep have been evaluated in the forensic medical context because violent behaviors can be associated with this parasomnia. Aim., To describe the clinical and polysomnographic findings in three patients who referred to our sleep laboratory for sleep disorders and who reported episodes of sleep-related sexual activation. Main Outcome Measures., We analyzed video-polysomnographic recordings, sleep structure, sleep microstructure, and sleep-related respiratory events. Methods., The patients were three males aged 42, 32, and 46 years. All had unremarkable medical, neurological, and psychiatric histories. All underwent full-night polysomnography. Results., Each patient presented a distinct sleep disorder: one had severe obstructive sleep apnea syndrome (OSAS), one presented clinical and polysomnographic features of non-rapid eye movement (NREM) sleep parasomnia (somnambulism), and the third presented clinical and polysomnographic features of rapid eye movement behavior disorder. Conclusions., In our patients, the clinical and polysomnographic findings suggest that abnormal nocturnal sexual behavior can occur in association with distinct sleep disorders, characterized by different pathophysiologic mechanisms and distinctive treatments. Abnormal sexual behaviors during sleep should be investigated with polysomnography in order to define their pathophysiology and to establish appropriate treatments. Della Marca G, Dittoni S, Frusciante R, Colicchio S, Losurdo A, Testani E, Buccarella C, Modoni A, Mazza S, Mennuni GF, Mariotti P, and Vollono C. Abnormal sexual behavior during sleep. J Sex Med 2009;6:3490,3495. 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