Effect of pregabalin on sleep structure of rats with temporal lobe epilepsy / 中华行为医学与脑科学杂志

Objective:To explore the effect of pregabalin on sleep structure in rats with temporal lobe epilepsy induced by pilocarpine.Methods:Twelve adult SD rats (half male and half female) were injected intraperitoneally with pilocarpine to establish a chronic temporal lobe epilepsy model.According to the principle of gender matching, they were divided into model group and pregabalin group, with 6 rats in each group(half male and half female). Another 6 SD rats (half male and half female) were taken as the control group.The skull electrodes were placed in the brain areas of rats to monitor the cerebral electrical activity, then recorded the data after resting for 1 week.Rats in pregabalin group were intraperitoneally injected with 50 mg/kg pregabalin while the rats in model group and control group were intraperitoneally injected with equal volume of normal saline.Fifteen minutes later, video electroencephalogram(EEG) and electromyogram(EMG) of rats in each group were recorded.The recording time was from 10∶00 to 17∶00 for 2 consecutive days.The seizure frequency, EEG and EMG were obtained.SPSS 25.0 was used for data analysis, one-way ANOVA was used for multi group comparison, and Tukey test and Games-Howell test were used for further pairwise comparison.Results:(1)The frequency of seizures in the pregabalin group (0.0(0.0, 1.0)times) were significantly lower than that in the model group(2.5(1.0, 4.8)times)( Z=-3.0, P<0.05). (2)During the 7 h recording period, the analyzed data showed that there were significant differences in the sleep-wake transition frequency, slow-wave sleep(SWS) phase duration, rapid eye movement (REM) sleep phase duration, total SWS time, total REM time and total sleep time among the three groups( F=10.5, 4.1, 13.0, 7.8, 4.4, 9.3, all P<0.05). The frequency of sleep-wake transitions in the pregabalin group ((66.3±18.0) times) and the control group ((87.8±14.1) times) were less than that in the model group ((106.7±20.8) times) (both P<0.05). The duration of SWS phase ((11.2±4.0) min) in pregabalin group was significantly longer than that in model group ((5.9±1.8) min) ( P<0.05), while that in model group was shorter than that in control group ((7.7±1.2) min) ( P<0.05). The duration of REM phase in the model group ((1.9±0.4) min) was shorter than that in the control group ((2.5±0.4) min) ( P<0.05). There was no significant difference in the duration of REM phase between the pregabalin group and the model group ( P>0.05). Within 7 h of observation, the total SWS time ((296.5±37.1) min) and total sleep time ((338.4±33.3) min) in pregabalin group were longer than those in model group ((258.1±38.4) min, (288.9±41.0) min) (both P<0.05). The total REM time ((30.4±11.1) min) and total sleep time ((288.9±41.0) min) in the model group were significantly shorter than those in the control group ((50.2±8.5) min, (339.0±19.6) min) (both P<0.05). Conclusion:Pregabalin alone can reduce seizures and change the sleep structure disorder caused by epilepsy, which is mainly manifested in reducing the number of sleep-wake transitions, prolonging the duration of SWS, increasing sleep duration, increasing SWS and total sleep time and improving sleep quality.

Alteraciones en el sueño por el consumo de cannabis / Sleep disturbances from the use of cannabis

RESUMEN Esta es una revisión de algunos ensayos clínicos realizados acerca de las repercusiones en la estructura, arquitectura y percepción del sueño en los consumidores de cannabis. Para la búsqueda bibliográfica se consultó bases de datos, con especial énfasis en revisiones sistemáticas, metaanálisis, estudios de cohortes, ensayos controlados aleatorios y estudios de casos y controles. Las palabras claves incluyeron términos que describen el uso del cannabis combinado con otros que se refieren al sueño o anormalidades del sueño (por ejemplo: sueño, insomnio, polisomnografía, tiempo total de sueño, latencia del sueño, sueño de onda lenta, sueño de movimiento ocular rápido y su latencia). Se extrajeron datos relevantes de cada uno de los artículos consultados. Se resumió la literatura disponible sobre mediciones subjetivas y objetivas, correlaciones clínicas y paraclínicas, diferencias entre el consumo agudo, crónico y la abstinencia, y otros puntos de discusión. Se realizaron varias correlaciones moleculares y anatómicas que explican los cambios en el sueño desde el punto de vista del sistema nervioso central. Finalmente, los resultados demuestran una disminución de la latencia del sueño con el uso agudo a dosis bajas, además menor tiempo de vigilia luego del inicio del sueño, aumento del sueño de ondas lentas y disminución del sueño de movimientos oculares rápidos; estos efectos no permanecen con el uso crónico, ya que posteriormente se presenta una peor calidad del sueño; el escenario también varía con la abstinencia, puede presentarse insomnio, disminución del tiempo total del sueño de onda lenta y del sueño total.

ABSTRACT This is a review of some clinical trials conducted on the impact on sleep structure, architecture and perception in cannabis users. For the literature search, consult database queries with special emphasis on systematic reviews, meta-analyzes, cohort studies, randomized controlled trials, and case-control studies. Keywords include terms that describe cannabis use combined with others that specify sleep or sleep abnormalities (for example: sleep, insomnia, polysomnography, total sleep time, sleep latency, slow wave sleep, motion sleep fast eyepiece and its latency). Relevant data was extracted in each of the articles consulted. The available literature is summarized on: subjective and objective measurements, clinical and paraclinical correlations, differences between acute and chronic consumption and abstinence, and other points of discussion. Tese are various molecular and anatomical correlations that explain changes in sleep from the point of view of the central nervous system. Finally, results frequently decrease sleep latency with acute use at low doses, plus shorter waking time after sleep onset, increased slow wave sleep and decreased rapid eye movement sleep, these effects do not persist with chronic use since later there is a worse quality of sleep; The setting also changes with abstinence where insomnia may occur, decreased total time for slow wave sleep and total sleep.

Does Rapid Eye Movement Sleep Aggravate Obstructive Sleep Apnea?

OBJECTIVES.: To investigate the apnea-hypopnea index (AHI) according to the sleep stage in more detail after control of posture. METHODS.: Patients who underwent nocturnal polysomnography between December 2007 and July 2018 were retrospectively evaluated. Inclusion criteria were as follows: age >18 years, sleep efficacy >80%, and patients who underwent polysomnography only in the supine position (100% of the time). Patients were classified into different groups according to the methods: the first, rapid eye movement (REM)-dominant group (AHIREM/AHINREM >2), non-rapid eye movement (NREM)-dominant group (AHINREM/AHIREM >2), and non-dominant group; and the second, light sleep group (AHIN1N2>AHISWS) and slow wave sleep (SWS) group (AHISWS>AHIN1N2). RESULTS.: A total of 234 patients (mean age, 47.4±13.9 years) were included in the study. There were 108 patients (46.2%) in the REM-dominant group, 88 (37.6%) in the non-dominant group, and 38 (16.2%) in the NREM-dominant group. The AHI was significantly higher in the NREM-dominant group than in the REM-dominant group (32.9±22.9 events/hr vs. 18.3±9.5 events/hr, respectively). There were improvements in the AHI from stage 1 to SWS in NREM sleep with the highest level in REM sleep. A higher AHISWS than AHIN1N2 was found in 16 of 234 patients (6.8%); however, there were no significant predictors of these unexpected results except AHI. CONCLUSION.: Our results demonstrated the highest AHI during REM sleep stage in total participants after control of posture. However, there were 16.2% of patients showed NREM-dominant pattern (AHINREM/AHIREM >2) and 6.8% of patients showed higher AHISWS than AHIN1N2. Therefore, each group might have a different pathophysiology of obstructive sleep apnea (OSA), and we need to consider this point when we treat the patients with OSA.

A Critical Time-Window for the Selective Induction of Hippocampal Memory Consolidation by a Brief Episode of Slow-Wave Sleep / 神经科学通报·英文版

Although extensively studied, the exact role of sleep in learning and memory is still not very clear. Sleep deprivation has been most frequently used to explore the effects of sleep on learning and memory, but the results from such studies are inevitably complicated by concurrent stress and distress. Furthermore, it is not clear whether there is a strict time-window between sleep and memory consolidation. In the present study we were able to induce time-locked slow-wave sleep (SWS) in mice by optogenetically stimulating GABAergic neurons in the parafacial zone (PZ), providing a direct approach to analyze the influences of SWS on learning and memory with precise time-windows. We found that SWS induced by light for 30 min immediately or 15 min after the training phase of the object-in-place task significantly prolonged the memory from 30 min to 6 h. However, induction of SWS 30 min after the training phase did not improve memory, suggesting a critical time-window between the induction of a brief episode of SWS and learning for memory consolidation. Application of a gentle touch to the mice during light stimulation to prevent SWS induction also failed to improve memory, indicating the specific role of SWS, but not the activation of PZ GABAergic neurons itself, in memory consolidation. Similar influences of light-induced SWS on memory consolidation also occurred for Y-maze spatial memory and contextual fear memory, but not for cued fear memory. SWS induction immediately before the test phase had no effect on memory performance, indicating that SWS does not affect memory retrieval. Thus, by induction of a brief-episode SWS we have revealed a critical time window for the consolidation of hippocampus-dependent memory.

Effect of long-term deep slow-wave sleep deprivation on the reproductive system in male rats / 中华劳动卫生职业病杂志

Objective@#To investigate the effect of long-term deep slow-wave sleep deprivation on the gonad axis, sperm abnormality rate, and structure of the testis in male rats and possible mechanisms.@*Methods@#A total of 30 specific pathogen-free male Wistar rats aged 5 weeks were randomly divided into slow-wave sleep deprivation group 1 (SD1 group) , slow-wave sleep and sleep time deprivation group 2 (SD2 group) , and control group, with 10 rats in each group. The flower pot method was used to establish a model of sleep deprivation. In addition to 12-hour sleep deprivation at night, the rats in the SD1 group were given interference once every 24 minutes, and those in the SD2 group were deprived of sleep for 8 minutes every 24 minutes; the rats in the control group were given 12-hour light illumination and then placed in dark environment for 12 hours. All rats were sacrificed by exsanguination from the femoral artery, and the testis, the epididymis, and blood were collected for analysis. Sperm abnormality rate and sperm motility rate were measured, and cauda epididymal sperm counting was performed. ELISA was used to measure the serum levels of testosterone (T) , follicle-stimulating hormone (FSH) , and luteinizing hormone (LH) .@*Results@#Compared with the control group, the SD2 group had a significant increase in organ coefficient of the epididymis (P<0.05) and a significant reduction in sperm motility rate (P<0.05) . There were significant differences between the SD1 group and the SD2 group in the increase in sperm abnormality rate (P<0.05) and the reduction in cauda epididymal sperm count (P<0.05) . The levels of FSH and T tended to increase, and the level of LH tended to decrease. Pathological examination showed degeneration and vacuolization of a small amount of spermatogenic cells in the SD1 group; in the SD2 group, there were significant degeneration, edema, and vacuolization of most spermatogenic cells, some spermatogenic cells were observed in the lumen, and there were no sperms in the lumen.@*Conclusion@#Long-term deep slow-wave sleep deprivation impairs the structure of the testis, affects sperm motility rate and sex hormones, and increases the risk of sperm abnormality.

Sleep architecture in drug naive patients with schizophrenia: A meta-analysis / 中国心理卫生杂志

Objective:To assess the characteristics change of sleep architecture in drug naive patients with schizophrenia,compared with healthy control.Methods:The key words including schizophrenia and sleep architecture (or sleep structure or sleep disturbance or polysomnogram and so on) were used to search literatures in MEDLINE,Embase,Springer,PsychINFO,google scholar,Wanfang data,published from 1980 to 2015.Fifteen studies that compared sleep architecture in drug naive patients with schizophrenia and healthy control were included.Literature quality evaluation was performed with the Newcastle-Ottawa Scale.The meta-analysis was performed by using Stata13.0 software.Results:Compared to healthy control,the total sleep time decreased (P ＜ 0.01),the sleep latency increased (P ＜ 0.01),the sleep efficiency decreased (P ＜ 0.01),and the rapid-eye-movemem (REM) sleep latency increased (P ＜ 0.01) significantly in drug naive patients with schizophrenia.The proportion of stage1 was increased,and the proportions of stage4 and slow wave sleep stage were decreased,the differences between case and control were statistically significant.Conclusion:In the control of drug effects,patients with schizophrenia may have poorer sleep quality of be poorer than healthy controls,such as the decreased total sleep time,specifically slow wave sleep,prolonged sleep latency and decreased sleep efficiency.

Effects of Isoflurane Anesthesia on Post-Anesthetic Sleep-Wake Architectures in Rats

The sleep homeostatic response significantly affects the state of anesthesia. In addition, sleep recovery may occur during anesthesia, either via a natural sleep-like process to occur or via a direct restorative effect. Little is known about the effects of isoflurane anesthesia on sleep homeostasis. We investigated whether 1) isoflurane anesthesia could provide a sleep-like process, and 2) the depth of anesthesia could differently affect the post-anesthesia sleep response. Nine rats were treated for 2 hours with ad libitum sleep (Control), sleep deprivation (SD), and isoflurane anesthesia with delta-wave-predominant state (ISO-1) or burst suppression pattern-predominant state (ISO-2) with at least a 1-week interval. Electroencephalogram and electromyogram were recorded and sleep-wake architecture was evaluated for 4 hours after each treatment. In the post-treatment period, the duration of transition to slow-wave-sleep decreased but slow wave sleep (SWS) increased in the SD group, but no sleep stages were significantly changed in ISO-1 and ISO-2 groups compared to Control. Different levels of anesthesia did not significantly affect the post-anesthesia sleep responses, but the deep level of anesthesia significantly delayed the latency to sleep compared to Control. The present results indicate that a natural sleep-like process likely occurs during isoflurane anesthesia and that the post-anesthesia sleep response occurs irrespective to the level of anesthesia.

Sleep, ageing and night work

Studies have shown that the frequency or worsening of sleep disorders tends to increase with age and that the ability to perform circadian adjustments tends to decrease in individuals who work the night shift. This condition can cause consequences such as excessive sleepiness, which are often a factor in accidents that occur at work. The present study investigated the effects of age on the daytime and nighttime sleep patterns using polysomnography (PSG) of long-haul bus drivers working fixed night or day shifts. A total of 124 drivers, free of sleep disorders and grouped according to age (<45 years, N = 85, and ≥45 years, N = 39) and PSG timing (daytime (D) PSG, N = 60; nighttime (N) PSG, N = 64) participated in the study. We observed a significant effect of bedtime (D vs N) and found that the length of daytime sleep was shorter [D: <45 years (336.10 ± 73.75 min) vs N: <45 years (398 ± 78.79 min) and D: ≥45 years (346.57 ± 43.17 min) vs N: ≥45 years (386.44 ± 52.92 min); P ≤ 0.05]. Daytime sleep was less efficient compared to nighttime sleep [D: <45 years (78.86 ± 13.30 percent) vs N: <45 years (86.45 ± 9.77 percent) and D: ≥45 years (79.89 ± 9.45 percent) and N: ≥45 years (83.13 ± 9.13 percent); P ≤ 0.05]. An effect of age was observed for rapid eye movement sleep [D: <45 years (18.05 ± 6.12 percent) vs D: ≥45 years (15.48 ± 7.11 percent) and N: <45 years (23.88 ± 6.75 percent) vs N: ≥45 years (20.77 ± 5.64 percent); P ≤ 0.05], which was greater in younger drivers. These findings are inconsistent with the notion that older night workers are more adversely affected than younger night workers by the challenge of attempting to rest during the day.

Childhood Parasomnia / 수면정신생리

Parasomnias are characterized by undesirable physical events or experiences during sleep. They occur alone or combined with other parasomnias. Parasomnias in childhood are more common than those of adulthood. Most of them are mild, benign and self remitted. Careful history takings from the patients and their parents, videotaped recordings of the episodes are invaluable to diagnose parasomnias. Sometimes polysomnographic recordings are helpful to differentiate ambiguous conditions and to diagnose comorbid conditions. Even many parasomnias do not need treatment, some conditions need therapeutic interventions. Medication, cognitive behavioral treatment, biofeedback, and oral appliance are helpful to reduce frequency and complexity of certain kinds of parasomnias.

Childhood Parasomnia / 수면정신생리

Parasomnias are characterized by undesirable physical events or experiences during sleep. They occur alone or combined with other parasomnias. Parasomnias in childhood are more common than those of adulthood. Most of them are mild, benign and self remitted. Careful history takings from the patients and their parents, videotaped recordings of the episodes are invaluable to diagnose parasomnias. Sometimes polysomnographic recordings are helpful to differentiate ambiguous conditions and to diagnose comorbid conditions. Even many parasomnias do not need treatment, some conditions need therapeutic interventions. Medication, cognitive behavioral treatment, biofeedback, and oral appliance are helpful to reduce frequency and complexity of certain kinds of parasomnias.