Alpha anteriorization and theta posteriorization during deep sleep.

Brain states (wake, sleep, general anesthesia, etc.) are profoundly associated with the spatiotemporal dynamics of brain oscillations. Previous studies showed that the EEG alpha power shifted from the occipital cortex to the frontal cortex (alpha anteriorization) after being induced into a state of general anesthesia via propofol. The sleep research literature suggests that slow waves and sleep spindles are generated locally and propagated gradually to different brain regions. Since sleep and general anesthesia are conceptualized under the same framework of consciousness, the present study examines whether alpha anteriorization similarly occurs during sleep and how the EEG power in other frequency bands changes during different sleep stages. The results from the analysis of three polysomnography datasets of 234 participants show consistent alpha anteriorization during the sleep stages N2 and N3, beta anteriorization during stage REM, and theta posteriorization during stages N2 and N3. Although it is known that the neural circuits responsible for sleep are not exactly the same for general anesthesia, the findings of alpha anteriorization in this study suggest that, at macro level, the circuits for alpha oscillations are organized in the similar cortical areas. The spatial shifts of EEG power in different frequency bands during sleep may offer meaningful neurophysiological markers for the level of consciousness.

Benzodiazepines and Sleep Architecture: A Systematic Review.

BACKGROUND: Insomnia, defined as a difficulty in initiating or maintaining sleep, is a relevant medical issue. Benzodiazepines (BZDs) are commonly prescribed to treat insomnia. Two phases characterize human sleep structure: sleep with Non-Rapid Eye Movement (NREM) and sleep with Rapid Eye Movement (REM). Physiological sleep includes NREM and REM phases in a continuous cycle known as "Sleep Architecture." OBJECTIVE: This systematic review summarizes the studies that have investigated effects of BZDs on Sleep Architecture. METHODS: The articles selection included human clinical trials (in English, Portuguese, or Spanish) only, specifically focused on BZDs effects on sleep architecture. PubMed, BVS, and Google Scholar databases were searched. RESULTS: Findings on BZDs effects on sleep architecture confirm an increase in stage 2 of NREM sleep and a decrease in time of stages 3 and 4 of NREM sleep with a reduction in time of REM sleep during the nocturnal sleep. CONCLUSION: Variations in NREM and REM sleep may lead to deficits in concentration and working memory and weight gain. The increase in stage 2 of NREM sleep may lead to a subjective improvement of sleep quality with no awakenings. BZDz should be prescribed with zeal and professional judgment. These patients should be closely monitored for possible long-term side effects.

Clinical and electrophysiological study of sleep-related hypermotor epilepsy during rapid eye movement sleep / 中华神经科杂志

Objective:To explore the electro-clinical characteristics of sleep-related hypermotor epilepsy (SHE) in rapid eye movement (REM) stage.Methods:Five patients of SHE in REM stage were studied and followed up in the Electroencephalogram Monitoring Center, Department of Neurology, Xijing Hospital, the Air Force Military Medical University, from January 2016 to August 2021.Results:Among the 5 patients, there are 3 male patients, aged 21 to 46 years. A total of 23 seizures were monitored in 5 patients, of which 22 occurred in REM sleep and 1 occurred in non-REM Ⅲ sleep. Each attack lasted from 30 seconds to 1 minute, and was manifested as "hyperkinetic attack" during sleep, with or without disturbance of consciousness. There were no obvious abnormalities in electroencephalography during 13 attacks, with the focal sharp slow waves or slow waves during 9 attacks, and the focal slow waves occurrence at the end of the 10 attacks.Conclusion:Most of the hypermotor epileptic seizures in REM stage started from awakening reaction, and the interictal discharges occured in waking and non-REM sleep stage, which is necessary to distinguish from the REM sleep behavior disorder.

Association of apnea-hypopnea index during rapid eye movement sleep with insulin resistance in patients with suspected obstructive sleep apnea: a cross-sectional study.

BACKGROUND: Obstructive sleep apnea (OSA) is associated with insulin resistance. However, the association between special stages of OSA [rapid eye movement (REM) sleep] and insulin resistance is not clear. This study was designed to assess the association of the frequency of respiratory events during REM sleep with insulin resistance in adults with suspected OSA. METHODS: In this cross-sectional study, 4,062 adult participants with suspected OSA who underwent polysomnography in our sleep center between 2009 and 2016 were screened. Polysomnographic variables, biochemical indicators, and physical measurements were collected. Logistic regression analyses were conducted to determine the odds ratios (ORs) and 95% confidence intervals (95% CIs) for insulin resistance as assessed by the presence of hyperinsulinemia, the homeostasis model assessment of insulin resistance (HOMA-IR) index, the fasting insulin resistance index (FIRI), and Bennett's insulin sensitivity index (ISI). RESULTS: The final analyses included 2,899 adults with suspected OSA. Multivariate adjustments, including the apnea-hypopnea index (AHI) during non-REM sleep (AHINREM), were performed. The AHI during REM sleep (AHIREM) was found to be independently associated with insulin resistance across increasing AHIREM quartiles. For hyperinsulinemia the ORs (95% CIs) followed the order of 1.340 (1.022, 1.757), 1.210 (0.882, 1.660), and 1.632 (1.103, 2.416). For abnormal HOMA-IR, ORs (95% CIs) were 1.287 (0.998, 1.661), 1.263 (0.933, 1.711), and 1.556 (1.056, 2.293). For abnormal FIRI, ORs (95% CIs) were 1.386 (1.048, 1.835), 1.317 (0.954, 1.818), and 1.888 (1.269, 2.807). For abnormal Bennett's ISI, ORs (95% CIs) were 1.297 (1.003, 1.678), 1.287 (0.949, 1.747), and 1.663 (1.127, 2.452). All linear trends were statistically significant (P<0.01). Additionally, the results showed that REM sleep duration was independently associated with hyperinsulinemia (OR =0.777, 95% CI: 0.615-0.982; P<0.05). CONCLUSIONS: AHIREM was independently associated with hyperinsulinemia and an abnormal HOMA-IR, FIRI, and Bennett's ISI in adults with suspected OSA. Additionally, REM sleep duration was independently associated with hyperinsulinemia.

Microinjection of melanin-concentrating hormone (MCH) into the median raphe nucleus promotes REM sleep in rats.

Melanin concentrating hormone (MCH) is a sleep-promoting neuromodulator synthesized by neurons located in the postero-lateral hypothalamus and incerto-hypothalamic area. MCHergic neurons have widespread projections including the serotonergic dorsal (DR) and median (MnR) raphe nuclei, both involved in the control of wakefulness and sleep. In the present study, we explored in rats the presence of the MCH receptor type 1 (MCHR-1) in serotonergic neurons of the MnR by double immunofluorescence. Additionally, we analyzed the effect on sleep of MCH microinjections into the MnR. We found that MCHR-1 protein was present in MnR serotonergic and non-serotonergic neurons. In this respect, the receptor was localized in the primary cilia of these neurons. Compared with saline, microinjections of MCH into the MnR induced a dose-related increase in REM sleep time, which was related to a rise in the number of REM sleep episodes, associated with a reduction in the time spent in W. No significant changes were observed in non-REM (NREM) sleep time. Our data strongly suggest that MCH projections towards the MnR, acting through the MCHR-1 located in the primary cilia, promote REM sleep.

Relationship between obstructive sleep apnoea during rapid eye movement sleep and metabolic syndrome parameters in patients with type 2 diabetes mellitus.

PURPOSE: Sleep-disordered breathing (SDB) is associated with hypertension, poor glycemic control and dyslipidemia. Usually, apnoea events tend to be more prominent during rapid eye movement (REM) sleep than non-REM (NREM) sleep. We examined which SDB parameters are associated with blood pressure (BP), HbA1c and lipid profile in patients with type 2 diabetes (T2D). METHODS: A total of 185 patients with T2D who underwent polysomnography were analysed. Exclusion criteria were: the presence of pulmonary diseases, central sleep apnoea, treated SDB, or REM sleep < 30 min. To predict BP, HbA1c, and lipid profiles, we performed multiple linear regression analyses adjusted for known risk factors. Subsequently, we performed multivariable logistic regression analyses. RESULTS: Patient characteristics (mean ± standard deviation/median) were as follows: age 58.0 ± 11.8 years, body mass index 26.0 kg/m2 (24.1-28.9 kg/m2 ), systolic BP 134 ± 19 mmHg, mean BP 98 ± 14 mmHg, HbA1c 7.4% (6.8-8.4%), triglyceride 143 mg/dL (97-195 mg/dL), non-high density lipoprotein (non-HDL) cholesterol 143 mg/dL (120-163 mg/dL), REM-apnoea-hypopnea index (AHI) 35.1/h (21.1-53.1/h). The analyses revealed that REM-AHI was independently associated with systolic and mean BP, whereas NREM-AHI was not. A statistically significant association was not observed between REM-AHI and HbA1c or lipid profile. CONCLUSION: In patients with T2D, REM-AHI was associated with systolic and mean BP. The alteration of BP, associated with SDB during REM sleep, may be an important pathophysiological link between SDB and cardiovascular diseases.

Clinical and electrophysiological study of neck myoclonus during sleep / 中华神经科杂志

Objective:To discuss the clinical and electrophysiological characteristics of neck myoclonus during sleep.Methods:The clinical and electrophysiological characteristics of 31 patients in the Electroencephalography Monitoring Center of Xijing Hospital from January 2020 to August 2020 were studied retrospectively. All the patients received video-polysomnography and video-electroencephalography.Results:There were 22 males (71%) and nine females (29%) in the 31 patients. The mean age of the patients at the time of inclusion in the study was 27.8 years. Neck myoclonus was most common in patients with narcolepsy ( n=8), followed by epilepsy ( n=4), obstructive sleep apnea syndrome ( n=4), anxiety and depression ( n=3), snoring ( n=3), etc. A total of 555 motor events were considered and analyzed, 89.5% (497/555) of which occurred during rapid eye movement (REM) sleep. The mean neck myoclonus index in REM sleep (5.8) was significantly higher than that in non-rapid eye movement sleep (0.2). Totally 48.3% (268/555) of neck myoclonus were accompanied by an arousal, 0.7% (4/555) by a full awakening, and 2.7% (15/555) by limb movements. Conclusions:Neck myoclonus is common during REM sleep, which can occur in patients with sleep disorders and epilepsy. Physiological or pathological significance of neck myoclonus has to be investigated in further studies.

REM-sleep related hypermotor seizures: Video documentation and ictal source imaging.

INTRODUCTION: Rapid eye movement (REM) sleep has an inhibitory effect on epileptiform EEG discharges, and seizures occur extremely rarely in REM sleep. CASE STUDY: We present the case and video recordings of a 10-year-old boy, with sleep-related hypermotor seizures starting from REM sleep, identified from videoEEG recordings. The semiology comprised intense fear, tachycardia, tachypnea, followed by hypermotor manifestations. Further investigations included brain MRI and source localization of the EEG signals. Multiple antiepileptic drugs were tried, the patient obtaining a good control of the seizures in the last 2.5 years with eslicarbazepine. DISCUSSION AND CONCLUSION: The ictal EEG source imaging showed seizure onset in the anterior part of the right insula, with propagation to the orbitofrontal area, confirmed by the semiological sequence. Although rare, focal seizures can be triggered by REM sleep and our findings suggest that deficient maturation of brain areas involved in sleep modulation might induce insufficient desynchronization during REM sleep, thus allowing seizure emergence.

Association between autophagy and rapid eye movement sleep loss-associated neurodegenerative and patho-physio-behavioral changes.

Rapid eye movement (REM) sleep is a unique physiological process at least expressed in mammals. Its disturbance affects many psycho-somato-physiological processes including cardio-vascular-respiratory systems, brain excitability, neurogenesis, synaptic pruning, and memory consolidation. While it is altered in most neurodegenerative disorders including Alzheimer's disease (AD), Parkinson's disease (PD) and REM sleep behavior disorder (RBD), the detailed mechanism of inducing such action is unknown. Independent studies have reported that by clearing unwanted, dysfunctional intracellular debris, wastes, etc., autophagy maintains cellular health, integrity, and homeostasis. Abnormality in autophagy causes neuronal dysfunction including death, leading to neurodegenerative disorders. It has also been reported that by modulating noradrenaline (NA) levels, REM sleep maintains neuronal integrity and house-keeping functions of the brain. Using PUBMED, we surveyed the literature and found isolated, independent studies showing that autophagy dysfunction is associated with acute and chronic neurodegenerative and patho-physio-behavioral changes, which are also associated with REM sleep loss. We collated these scattered findings, which strongly support our contention that elevated NA associated with REM sleep loss is likely to affect autophagy in neurons, disturbing neuronal integrity and homeostasis and leading to altered brain functions and associated disorders.

Thermo-parasomnia. Prediction of a possible sleep disorder or entity.

Parasomnias are a group of sleep disorders that are characterized by the presence of undesirable behavioral, experiential, or autonomic nervous system events during sleep initiation, within sleep, or during arousals from any stage of non-rapid eye movement (NREM) or rapid eye movement (REM) sleep. During wakefulness and NREM sleep, the hypothalamus plays a central role in thermoregulation. REM sleep has a very distinct thermoregulatory response that is characterized by an inhibition of hypothalamic control over body temperature, with resulting poikilothermia. The role of the thermoregulatory features of REM sleep is currently unknown. Drawing conclusions from other parasomnias one can assume that a disorder could exist in which the thermoregulatory features of REM sleep are impaired. The existence of this condition may have eluded current research because most of the research on thermoregulation has been completed using animal models or healthy volunteers. If this disorder were to exist, it could be associated with metabolic disorders, or with neurodegenerative conditions, and perhaps it could be an early biomarker for alpha-synucleinopathies in idiopathic REM sleep behavior disorder. New and evolving wearable technologies offer the promise of facilitating the monitoring of core body temperature and the testing of this hypothesized thermoregulatory autonomic disorder and its clinical correlates.

Coxsackie B2 Virus Infection Causing Multiorgan Failure and Cardiogenic Shock in a 42-Year-Old Man.

Infections from coxsackie B2 viruses often cause viral myocarditis and, only rarely, multisystem organ impairment. We present the unusual case of a 42-year-old man in whom coxsackie B2 virus infection caused multiorgan infection, necessitating distal pancreatectomy, splenectomy, renal dialysis, and venoarterial extracorporeal membrane oxygenation with mechanical ventilation. In addition, the patient had a rapid-eye-movement sleep-related conduction abnormality that caused frequent sinus pauses of longer than 10 s, presumably due to myocarditis from the coxsackievirus infection. He recovered after permanent pacemaker placement and was discharged from the hospital. We discuss our aggressive supportive care and the few other reports of multiorgan impairment from coxsackieviruses.

The association between obstructive sleep apnea during REM sleep and autonomic dysfunction as measured by heart rate variability.

PURPOSE: To determine the effect of obstructive sleep apnea (OSA) during rapid eye movement (REM) sleep on autonomic dysfunction using heart rate variability (HRV) analysis. METHODS: The medical records of adults who underwent nocturnal polysomnography at the Sleep and Chronobiology Center at Seoul National University Hospital were retrospectively reviewed. HRV parameters (mean RR interval, the standard deviation of all normal RR intervals [SDNN], square root of the mean squared differences of adjacent RR intervals [RMSSD], normalized low frequency [LF], normalized high frequency [HF], and the ratio of LF to HF [LF/HF]) were measured in 5-min electrocardiogram recordings obtained during W, N2, and R sleep stages. Comparisons were made among the control (apnea-hypopnea index (AHI < 15 and AHI during REM sleep (AHIREM) < 15, n = 27), REM-associated OSA (AHI < 15 and AHIREM ≥ 15, n = 27), and OSA (AHI ≥ 15, n = 27) groups. The groups were matched for age, sex, and body mass index. RESULTS: No significant differences were observed between the control and the REM-associated OSA groups for any of the HRV parameters. In contrast, compared with controls, the OSA group showed significantly lower normalized HF (p = 0.031) and higher LF/HF (p = 0.018) in stage W and a significantly shorter mean RR interval (p = 0.046) and lower RMSSD (p = 0.034) in stage N2. CONCLUSIONS: Our findings suggest that OSA during REM sleep is not a major contributor to autonomic dysfunction.

Associations Between Characteristics of Obstructive Sleep Apnea and Nocturnal Blood Pressure Surge.

Research suggests that oxygen desaturation and sleep stage during obstructive sleep apnea (OSA) are related to the magnitude of high blood pressure (BP) in a laboratory setting. However, in a clinical setting, these associations have not been well studied. We used a noninvasive oscillometric BP measurement device to investigate the association between oxygen-triggered BP levels at the end of each OSA episode and the characteristics of the preceding OSA episode. In 42 newly diagnosed OSA patients (average age, 63.5±12.5 years; average apnea-hypopnea index, 32.6±18.2 per hour), 258 BP measurements were obtained at the end of OSA episodes. Hypoxia-peak systolic BP (SBP), defined as the maximum oxygen-triggered SBP value, was significantly higher in rapid eye movement sleep (144.9±19.9 mm Hg) than in non-rapid eye movement stage 1 sleep (129.5±15.1 mm Hg; P<0.001) and non-rapid eye movement stage 2 sleep (129.4±14.7 mm Hg; P<0.001). In a multivariate-linear mixed model, the lowest oxygen saturation percentage during each OSA episode was associated with increased hypoxia-peak SBP (-0.501 mm Hg; P<0.001), nocturnal SBP surge (-0.395 mm Hg; P<0.001), defined as the difference between the hypoxia-peak SBP and the mean nocturnal SBP, and maximum value of SBP surge (-0.468 mm Hg; P<0.001), defined as the difference between the hypoxia-peak SBP and the minimum nocturnal SBP independent of sleep stage. These values were not associated with the duration of each OSA episode. The contribution of rapid eye movement sleep and severe oxygen desaturation to OSA-related BP elevation measured with a noninvasive oscillometric method was determined in a clinical setting.

Circadian rhythms of melatonin and peripheral clock gene expression in idiopathic REM sleep behavior disorder.

OBJECTIVE: To evaluate changes in the expression of clock genes and melatonin levels in patients with idiopathic REM sleep behavior disorder (RBD) as a potential early stage of synucleinopathies. METHODS: We assessed the rhythmicity of circadian clock genes using real time-quantitative polymerase chain reaction and 24-h blood melatonin profiles using radio-immunoassay in 10 RBD patients and nine age-matched controls. RESULTS: The RBD patients did not show circadian rhythmicity for clock genes Per2, Bmal1, and Nr1d1 but the rhythmicity of Per 1 remained, and the amplitude of Per3 was diminished. The 24-h melatonin rhythm did not differ between RBD patients and healthy control subjects. Melatonin profile in RBD patients was delayed by 2 h compared to controls, the habitual sleep phases were phase delayed by about 1 h, however no phase shift occurred in any of the clock genes studied. The control group had stable acrophases of melatonin rhythms of approximately 5 h whereas the RBD patients had a more dispersed range over 11 h. CONCLUSIONS: Our results suggest that RBD could be associated with altered expression of clock genes and delayed melatonin secretion. Thus, we argue that circadian system dysregulation could play a role in RBD.

Rapid Eye Movement sleep deprivation of rat generates ROS in the hepatocytes and makes them more susceptible to oxidative stress.

BACKGROUND: Rapid Eye Movement sleep deprivation (REMSD) of rats causes inflammation of the liver and apoptotic cell death of neurons and hepatocytes. Studies also suggest that REM sleep deprivation can cause muscle as well as cardiac injury and neurodegenerative diseases. OBJECTIVE AND METHODS: The aim of this research was to determine whether REM sleep deprivation of rats would increase the levels of reactive oxygen species (ROS) in the hepatocytes and create oxidative stress in them. We selectively deprived the rats for REM sleep using the standard flower pot method. RESULTS: We observed that when rats were subjected to REM sleep deprivation, the levels of ROS in their hepatocytes increased ~184.33% compared to large platform control (LPC) group by day 9 of deprivation, but it returned towards normal level (~49.27%) after recovery sleep for 5 days. Nitric oxide synthase (iNOS) gene expression and protein levels as determined by real-time PCR and western blot analysis respectively were found to be elevated in hepatocytes of REM sleep deprived rats as compared to the LPC group. The level of nitric oxide (NO) in the hepatocytes of REMSD rats also increased by ~404.40% as compared to the LPC group but sleep recovery for 5 days normalized the effect (~135.35% compared to LPC group). We used a large platform control group as a reference group to compare with the REM sleep deprived group as the effect on the hepatocytes of both LPC group and cage control groups were not significantly different. DISCUSSION: We have analyzed the oxidative stress generated in the hepatocytes of rats due to REM sleep deprivation and further consequences of it. REMS deprivation not only increased the levels of ROS in the hepatocytes but also induced iNOS and NO in them. REM sleep deprived hepatocytes became more susceptible to oxidative stresses on further exposures. Furthermore, our study has great pathological and physiological.

Analysis of characteristics of polysomnography in patients with multiple dreams / 中华神经科杂志

Objective To investigate the characteristics of sleep structures in patients with multiple dreams through the retrospective analysis of polysomnography in patients with multiple dreams,and to provide a theoretical basis for the treatment of multiple dreams.Methods Twenty-two cases with multiple dreams in Department of Neurology,the People's Hospital of Zhengzhou University from July 2015 to Ferbuary 2018 were included in multi-dream group and 12 healthy people in control group.The sleep parameters related to polysomnography during the visit were collected and recorded,and the differences between the two groups were compared.Resluts There was no statistically significant difference in apneahypopnea index,sleep latency,rapid eye movement (REM) sleep latency,slow-wave sleep ratio,and REM-arousal index between the two groups.Compared with the control group,sleep efficiency (73.46％ ± 12.41％ vs 90.43％ ± 4.42％,t=-4.555,P=0.000),REM period ratio (16.28％ ± 5.59％ vs 21.59％ ± 2.70％,t =-3.727,P =0.001) decreased in the multi-dream group;whereas ratio of light sleep (66.49％ ±9.97％ vs 59.85％ ±3.01％,t =2.966,P =0.006),awakening numbers (13.4 ±6.98 vs 6.08 ± 3.34,t =3.411,P =0.002),arousal index (20.11 ± 10.69 vs 11.82 ± 8.09,t =2.338,P =0.026),non-REM arousal index (20.22 ± 10.53 vs 12.08 ± 8.69,t =2.283,P =0.029) increased.Conclusion The sleep efficiency of patients with multiple dreams is reduced,and their perceived dreams may originate from light sleep periods.

Abnormal functional connectivity of the cores that control rapid eye movement sleep in idiopathic rapid eye movement sleep behavior disorder / 中华神经科杂志

Objective To investigate the abnormal functional connectivity (FC) between the cores (including sublaterodorsal nucleus (SLD) and ventrolateral periaqueductal gray matter (vlPAG)) and the whole brain in rapid eye movement sleep behavior disorder (RBD) by resting state functional magnetic resonance imaging (rfMRI).Methods A total of 41 subjects recruited in the Department of Neurology,the People's Hospital of Zhengzhou University were enrolled in this study according to international diagnosis criteria,including 20 with idiopathic RBD (iRBD group) and 21 age,sex-matched normal controls (control group).All subjects were examined by Hoehn-Yahr Staging,cognitive tests and rfMRI.Resluts HoehnYahr staging score was 0(0,0) in the iRBD group,which showed no significant difference from that in the control group (0 (0,0),Z =-1.820,P =0.069).The scores of Rey Auditory Verbal Learning Test (AVLT) N1,AVLT N2,Symbol Digital Modalities Test,Rey-Osterrieth Complex Figure Test-Copy were 3.80 ± 1.67,5.10 ± 1.77,33.00(31.25,34.00) and 22.00(20.25,26.00) respectively in the iRBD group,which were significantly lower than that in the control group (4.95 ± 1.28,t =2.482,P =0.017;6.43±1.16,t =2.848,P=0.007;33.00(29.50,35.50),Z=-3.792,P=0.000;35.00(33.00,36.00),Z =-2.351,P =0.019) respectively.The scores of Trail Making Test 1 (86.5 (70.0,100.0))and Trail Making Test 2 (197.0(180.5,211.5)) in the iRBD group were significantly higher than that in the control group (66.0(49.0,91.5),112.0(99.5,173.0) respectively,Z=-2.373,P=0.018;Z =-3.105,P =0.002).Compared with the control group,the FC analysis showed reduced connections from the right SLD to the bilateral cingnlate gyrus (t =-4.173) and bilateral frontal gyrus (t =-2.965(left),-3.662(right)),from the vlPAG to the left precentral-postcentral gyrus(t =3.930),and from the vlPAG to the right frontal gyrus (t =4.141) in the iRBD.There was no statistically significant difference from the left SLD to the whole brain.Conclusion There were abnormal FCs from the SLD and vlPAG to cognitive and motor areas in RBD patients,perhaps leading to clinical RBD symptoms such as cognitive deterioration and movement disorder.

[Changes to sleep patterns in young migrants at high altitude].

Objective: To explore the relationship between the level of acclimatization and the changes to sleep architecture in migrants at high altitude. Methods: Nocturnal sleep recordings of 50 subjects aged between 18 and 25 years [mean age (20.9±2.0) years] were analyzed. Those young volunteers were divided into 3 700 m-3 m group(n=10, migrated to an altitude of 3 700 metres for 3 months), 3 700 m-1 y group(n=10, for 1 year) , 5 380 m-3 m group(n=8), 5 380 m-1 y group(n=9), and compared with a control group(n=13, at 1 400 m altitude). Results: When the migrants stayed at 5 380 m for 3 months or 1 year, the wake time increased significantly during sleep[(81.81±59.80)min vs(47.19±24.98) min, P=0.026; (77.94±25.64)min vs(47.19±24.98)min, P=0.040]. Concerning the percentage of total sleep time(TST) in each stage, participants in the 5 380 m-3 m group had a shift in sleep stage distribution with near absence of slow wave sleep(SWS) and a significant increase of N1 , but N2 and rapid eye movement(REM) did not differ. Interestingly, there were entirely concordant changes among the other 3 groups of results, decreased N2 and increased REM. Conclusions: The migrants' abilities to acclimatize themselves to plateau were varied according to the arrived altitude and the length of stay. The sleep of short- time migrants was characterized by increased N1 and decreased SWS, whereas that of well acclimatized migrants was characterized by less N2 and more REM. The efficient recovery in SWS may be an objective reference in high altitude acclimatization.

Parasomnias en Pediatría: Una visión clínica / Parasomnia in Pediatrics: A clinical view

Resumen Un motivo frecuente de consulta, en la práctica pediátrica, son los trastornos del sueño que pueden afectar hasta al 30% de la población infantil, con repercusiones negativas tanto en el aspecto cognitivo como conductual y físico (Meijer et al. 2000). Dentro de estas manifestaciones se encuadran las denominadas parasomnias que son fenómenos o manifestaciones anormales, molestas o displacenteras, que se presentan durante las etapas del sueño y se pueden acompañar de cambios siológicos cardiovasculares y/o motores. Constituyen un tercio de todos los trastornos del sueño con causas relacionadas al neurodesarrollo o a patrones familiares y desencadenantes similares (medicamentos, ebre, trastornos respiratorios y stress). Particularmente cuando coexisten con trastornos neurológicos o del neurodesarrollo, pudiendo confundirse con otras patologías tal como la epilepsia, lo que conlleva un desafío diagnóstico para el Neuropediatra. Corresponden a la tercera causa de alteraciones de sueño en la infancia con origen tanto en factores genéticos con patrones ligados a la herencia y otras se asociadas al neurodesarrollo del SNC. Se las clasifica, según en qué etapa del sueño se presentan en: Trastornos del Alertamiento, Trastornos de la Transición sueño/vigilia, Trastornos asociados al sueño REM y otras parasomnias. Existen cada vez más evidencias acerca de los efectos de la inadecuada higiene se sueño y problemas del neurodesarrollo que nos obligan a echar más luz sobre esta problemática para corregir y evitar problemas futuros asociadas a ello, siendo el propósito de este trabajo el realizar una revisión sobre los conocimientos actuales sobre el tema en cuestión.

Abstract A frequent chief complaint in pediatric practice are sleep disorders, which may affect up to 30% of the pediatric population. These may have harmful e ects on cognition, behavior and physical development (Meijer et al. 2000). These sleep disorders include parasomnias, unpleasant abnormal phenomena that occur during sleep and may be accompanied by cardiovascular and/or motor manifestations. These make up one third of all sleep disorders caused by disturbances of neural development or family patterns, with similar triggering factors, such as medication, fever, respiratory disorders and stress. When they coincide with neurological or neural development disorders they may be confused with other disease conditions, such as epilepsy, and be a diagnostic challenge for the pediatric neurologist. Parasomnias are the third cause of sleep disorders of childhood, originating in both hereditary genetic factors and others pertaining to neural development of the CNS. They are classified according to the stage of sleep they affect: disorders of waking, disorders of the sleep/waking transition, REM sleep associated disorders and other parasomnias. A growing body of evidence points to the effects of inadequate sleep hygiene and disorders of neural development, requiring, therefore, further research. This paper reviews current knowledge on the subject.

Effects of Optogenetic inhibition of BLA on Sleep Brief Optogenetic Inhibition of the Basolateral Amygdala in Mice Alters Effects of Stressful Experiences on Rapid Eye Movement Sleep.

Study Objectives: Stressful events can directly produce significant alterations in subsequent sleep, in particular rapid eye movement sleep (REM); however, the neural mechanisms underlying the process are not fully known. Here, we investigated the role of the basolateral nuclei of the amygdala (BLA) in regulating the effects of stressful experience on sleep. Methods: We used optogenetics to briefly inhibit glutamatergic cells in BLA during the presentation of inescapable footshock (IS) and assessed effects on sleep, the acute stress response, and fear memory. c-Fos expression was also assessed in the amygdala and the medial prefrontal cortex (mPFC), both regions involved in coping with stress, and in brain stem regions implicated in the regulation of REM. Results: Compared to control mice, peri-shock inhibition of BLA attenuated an immediate reduction in REM after IS and produced a significant overall increase in REM. Moreover, upon exposure to the shock context alone, mice receiving peri-shock inhibition of BLA during training showed increased REM without altered freezing (an index of fear memory) or stress-induced hyperthermia (an index of acute stress response). Inhibition of BLA during REM under freely sleeping conditions enhanced REM only when body temperature was high, suggesting the effect was influenced by stress. Peri-shock inhibition of BLA also led to elevated c-Fos expression in the central nucleus of the amygdala and mPFC and differentially altered c-Fos activity in the selected brain stem regions. Conclusions: Glutamatergic cells in BLA can modulate the effects of stress on REM and can mediate effects of fear memory on sleep that can be independent of behavioral fear.