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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.
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Objective:To investigate the motor and non-motor symptoms and polysomnographic features in patients with rapid eye movement sleep behavior disorder (RBD), early Parkinson's disease (PD) with and without RBD.Methods:Patients with idiopathic RBD (IRBD) and early PD were collected from the clinics in West China Hospital of Sichuan University from August 2020 to May 2021.All the patients were divided into 3 groups including IRBD group (67 cases), PD with RBD (PD+ RBD) group (19 cases), and PD without RBD (PD-RBD) group (22 cases). Unified Parkinson's disease rating scale part 3 (UPDRS-Ⅲ), Hoehn-Yahr(H-Y) stage, Epworth sleepiness scale (ESS), REM sleep behavior disorder questionnaire-Hong Kong (RBDQ-HK), 17-item Hamilton depression scale(HAMD-17), mini-mental state examination(MMSE), Sniffin’Sticks olfactory function test, visual analogue scale (VAS), and scale for outcomes in Parkinson's disease-AUT(SCOPA-AUT) were used to assess the motor and non-motor symptoms including sleepiness, RBD, depression, cognitive function, olfactory function, pain and autonomic function respectively.All patients were performed to the polysomnography (PSG) examination.One-way ANOVA, Krukal-Wallis test, χ2 test and Fisher accurate test were used to analyze the data of motor and non-motor symptoms and sleep parameters among the 3 groups accordingly. Results:There were statistically significant differences in motor symptoms among the three groups ( F=57.009, P<0.05), and the scores of UPDRS Ⅲ and H-Y stage were higher in the PD+ /- RBD group than those in the IRBD group(both P<0.05). However, there was no significant difference in motor symptoms between PD+ RBD group and PD-RBD group ( P>0.05). There were no significant differences in the scores of ESS, MMSE, olfactory function test and VAS (all P>0.05). But the HAMD-17 score was significantly higher in the PD+ RBD group(2(1, 9)) than that in the IRBD group (0(0, 3)( P<0.05). The SCOPA-AUT scores of autonomic function were significant differences in the three groups, mainly in the digestive system, urinary system, and sexual function ( P<0.05). Notably, the IRBD group (8(4, 14)) and PD+ RBD group (11(7, 14)) had higher scores of SCOPA-AUT compared with PD-RBD group (4(4, 5.75)(all P<0.05), especially in the digestive dysfunction(all P<0.05). The PD+ RBD group(3.47±1.17) had higher scores of sexual function compared with IRBP group(1.78±0.60)( P<0.05), and the urinary system scores also higher than PD-RBD group( P<0.05). The PD-RBD group(21.30 (6.10, 34.00)/h) had a significantly higher oxygen desaturation index in REM sleep compared with that of IRBD group(5.90(2.70, 16.73)/h) ( P<0.05). Conclusions:Early PD with RBD has more severe non-motor symptoms, especially depression and autonomic dysfunction.RBD can be related with the earlier and more widely autonomic dysfunction.
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Aiming at the limitations of clinical diagnosis of Parkinson's disease (PD) with rapid eye movement sleep behavior disorder (RBD), in order to improve the accuracy of diagnosis, an intelligent-aided diagnosis method based on few-channel electroencephalogram (EEG) and time-frequency deep network is proposed for PD with RBD. Firstly, in order to improve the speed of the operation and robustness of the algorithm, the 6-channel scalp EEG of each subject were segmented with the same time-window. Secondly, the model of time-frequency deep network was constructed and trained with time-window EEG data to obtain the segmentation-based classification result. Finally, the output of time-frequency deep network was postprocessed to obtain the subject-based diagnosis result. Polysomnography (PSG) of 60 patients, including 30 idiopathic PD and 30 PD with RBD, were collected by Nanjing Brain Hospital Affiliated to Nanjing Medical University and the doctor's detection results of PSG were taken as the gold standard in our study. The accuracy of the segmentation-based classification was 0.902 4 in the validation set. The accuracy of the subject-based classification was 0.933 3 in the test set. Compared with the RBD screening questionnaire (RBDSQ), the novel approach has clinical application value.
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Humans , Electroencephalography , Intelligence , Parkinson Disease/diagnosis , Polysomnography , REM Sleep Behavior Disorder/diagnosisABSTRACT
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.
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To explore the mechanism of rapid eye movement (REM) sleep regulation and the drugs that affect it. This article summarizes the relevant nucleuses regulating REM sleep in the pontine, medulla, and hypothalamus starting from the neural circuit that regulates REM sleep. Drugs that affect REM sleep, such as selective norepinephrine reuptake inhibitors and selective 5-hydroxytryptamine (5-HT) reuptake inhibitors, etc. The mechanism of action can be summarized as reducing the degradation of norepinephrine and 5-HT of synaptic sites, prolonging the action time of neurotransmitters, reducing the reuptake of presynaptic membrane, prolonging the action time of transmitters in the synaptic space, and relatively increasing norepinephrine and 5-HT neurons excitement.
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Objective@#To observe the influence of transcranial direct current stimulation (tDCS) on rapid eye movement sleep disorders among Parkinson′s disease (PD) patients.@*Methods@#Fifty-four PD patients were randomly divided into a treatment group (n=28) and a control group (n=26). Both groups were given routine drug treatment and nursing, while the treatment group was additionally provided with tDCS therapy. Both groups were evaluated using polysomnography (PSG), the Hamilton depression scale (HAMD), the pediatric daytime sleepiness scale (PDSS), the Epworth sleeping scale (ESS) and PD quality of life questionnaire-39 (PDQ-39) before and after four months of treatment.@*Results@#There were no significant differences between the two groups before the treatment. After the treatment, significant improvement was observed in the total sleep time (TST), sleep latency (SL), sleep efficiency (SE), rapid eye movement sleep (REMS), arousal index (AI), and in the HAMD, ESS, PDSS and PDQ-39 scores among the treatment group. In the control group only the average TST and HAMD score improved significantly. After the treatment, all of the treatment group′s average results were significantly better than the control group′s averages.@*Conclusion@#tDCS can significantly improve the sleep quality of patients with PD and relieve any depression, bettering their life quality.
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OBJECTIVE@#To investigate the effect of obstructive sleep apnea (OSA) on different sleep stages, and the relationship between N3 stage of non-rapid eye movement sleep and respiratory abnormal events.@*METHODS@#A total of 188 adult patients who underwent overnight polysomnography(PSG)monitoring in Sir Run Run shaw Hospital of Zhejiang University from June 24th to December 26th 2019 were enrolled in the study. OSA patients were classified into 3 groups (mild, moderate and severe) according to the apnea-hypopnea index (AHI). PSG data, AHI and the lowest SPO in each stage of sleep were compared among three groups.@*RESULTS@#There was no significant difference in total sleep time and sleep efficiency among patients with different severity of OSA (all >0.05). The proportion of N3 stage in moderate and severe OSA groups were significantly smaller than that in mild OSA group (all <0.05). The proportion of N3 stage in severe OSA group was also smaller than that in moderate OSA group (<0.05). In addition, severe OSA group had a longer latency of N3 stage than mild and moderate OSA groups (all <0.05). The latency of N3 stage in moderate OSA group was longer than that in mild OSA group (<0.05). The AHI in N3 stage was markedly lower than that in other sleep stages (all <0.01), regardless of the severity of OSA. Supine AHI in N3 stage in mild and moderate groups was significantly lower than that in N1, N2 and rapid eye movement (REM) stages (all <0.01). Supine AHI in N3 stage in severe group was also lower than that in N2 and REM stages (<0.05 or <0.01). The lowest SPO in N3 stage was significantly higher than that in N1, N2 and REM stages (<0.05 or <0.01), regardless of the severity of OSA.@*CONCLUSIONS@#s The proportion of N3 stage is lower in OSA patients, and N3 stage has less sleep respiratory events than non-N3 stages. The results suggest that the increased N3 stage proportion may indicate less severity of OSA.
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Las investigaciones recientes demuestran que mientras estamos tranquilamente durmiendo nuestro cerebro está muy ocupado procesando la información obtenida a lo largo del día. Asimismo, la falta de sueño ocasiona problemas en la consolidación de la memoria. El sueño juega un papel fundamental en el adecuado desarrollo del cerebro en crecimiento y muchos de los fenómenos de plasticidad cerebral ocurren durante el sueño. A nivel celular, los ciclos circadianos coordinan complejos mecanismos de "encender y apagar" genes y estructuras que regulan individualmente y colectivamente las funciones de cada célula del organismo y a su vez de cada órgano, cada sistema fisiológico, para finalmente producir un perfecto equilibrio en el funcionamiento mental, emocional y sistémico del individuo. El sueño influye en los procesos de memoria, aprendizaje, estados de ánimo y comportamiento, en las respuestas inmunológicas, procesos metabólicos, niveles de hormonas, digestión y muchas más funciones fisiológicas. Aquí presentamos una breve revisión de tres aspectos fundamentales relacionados con el sueño, enfocado especialmente en el efecto que tienen en procesos de aprendizaje y memoria: a. actividad eléctrica cerebral durante el sueño y correlación neuroanatómica con los mecanismos fisiológicos de memoria y aprendizaje; b. ciclos circadianos y su importancia en el funcionamiento de diferentes sistemas fisiológicos; c. algunos ejemplos de trastornos clínicos asociados con trastornos del sueño y sus repercusiones en aprendizaje y memoria.
Recent studies have demonstrated that while we are sleeping, our brain is very busy processing all information we have acquired along the day. Lack of sleep has shown to produce deficits in memory consolidation and plays an important role in brain development and brain plasticity in the several developmental stages of the human brain. At the cellular level, circadian cycles coordinate complex mechanism that "turn on and off" genes and cellular structures regulating individual cell functions to impact global organ and systems physiological activities. At the end a perfect and coordinated equilibrium in the mental, emotional and physiological is the goal of this complex process. Sleep impacts memory, learning, mood, behavior, immunological responses, metabolism, hormone levels, digestive process and many more physiological functions. We present a review of three basic aspects related with sleep: a. brain electrical activity during the sleep and neuroanatomic correlation with mechanism related with memory and learning; b. circadian cycles and impact in several physiological systems; c some examples of clinical disorders associated with sleep disorders and impact in learning and memory.
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Humans , Sleep/physiology , Circadian Rhythm/physiology , Learning/physiology , Memory/physiology , Neuronal Plasticity/physiology , Sleep Wake Disorders/physiopathology , Brain/physiology , Emotions/physiologyABSTRACT
Objective To explore the sleep structure characteristics and risk factors in patients with Parkinson disease psychosis (PDP).Methods Fifty-one patients with Parkinson disease were enrolled.Sixteen cases met the diagnostic criteria of Parkinson disease psychosis were included in the PDP group,while the remaining 35 cases were included in the PD group as the control group.Sleep status was monitored by polysomnography.Neuropsychological assessment of patients with Parkinson disease was performed by Parkinson quality of life questionnaire,Montreal cognitive assessment(MoCA)and Hoehn-Yahr state (H-Y) of Parkinson disease.Results There were statistically significant differences in age of onset in PD group and PDP group (64.11±8.87,57.44±10.07,t=1.242),course of disease (2 (1,4),6 (4,7),Z=-3.888),HY stage (2 (1.5,2.5),3 (2,3),Z=-2.487)(all P＜0.05).The total sleep time in the PDP group was lower than that in the PD group ((344.06±26.39)min,(361.74± 17.16)min,P＜0.05).Compared with the PD group,the proportion of slow wave sleep phase Ⅰ in the PDP group was bigger ((42.88 ± 7.99) ％,(37.14±5.21) ％,t=-3.065),and the proportion of slow wave sleep phase Ⅱ in the PDP group was smaller ((31.19±5.92) ％,(37.51±5.70) ％,t=3.634) (P＜0.05).Single factor binary logistic regression analysis showed that the course of disease,age of onset,RBD,HY stage,PDQ-39 questionnaire score,total sleep time,slow wave sleep stage Ⅰ (％) and slow wave sleep stage Ⅱ (％) were the risk factors of PDP (P＜0.05).Multivariate binary logistic regression analysis showed that the course of disease and RBD were independent risk factors for patients with PDP (P＜ 0.05).Conclusion Sleep structure changes in patients with PDP,and RBD is the independent risk factor for patients with Parkinson's psychotic disorders.
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Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by sleep interruption or trauma due to abnormal behaviors that occur during REM sleep. The pathophysiology of RBD is known to be a dysfunction of brainstem circuit that causes the loss of skeletal muscle atonia during REM sleep. The diagnosis of RBD is needed to confirm REM sleep without atonia in the polysomnography. The management of RBD includes not only drug treatment, but also to prevent injury from RBD and to follow-up on neurodegenerative diseases that may occur later. RBD is thought to be a prodromal stage of neurodegenerative disease associated with α-synucleoinopathy, such as Parkinson's Disease or multiple system atrophy. This article reviews the symptoms, epidemiology, diagnosis and treatment of RBD, the relevance of neurodegenerative diseases, and recent research trends.
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Brain Stem , Diagnosis , Epidemiology , Follow-Up Studies , Multiple System Atrophy , Muscle, Skeletal , Neurodegenerative Diseases , Parasomnias , Parkinson Disease , Polysomnography , Prodromal Symptoms , REM Sleep Behavior Disorder , Sleep, REMABSTRACT
<p><b>Background</b>Rapid eye movement (REM) sleep behavior disorder (RBD) and obstructive sleep apnea (OSA) are the most common sleep disorders in Parkinson's disease (PD). The aim of this study was to identify whether RBD could alleviate OSA severity in PD patients and its effect on cognitive impairment.</p><p><b>Methods</b>From February 2014 to May 2017, we recruited 174 PD patients from the Second Affiliated Hospital of Soochow University, all of whom underwent polysomnography (PSG). We collected clinical data, PSG results, and compared information between patients with and without RBD or OSA by analysis of covariance. We also investigated the effect of these sleep disorders on cognitive impairment using linear regression.</p><p><b>Results</b>We grouped participants as follows: PD only (n = 53), PD + OSA (n = 29), PD + RBD (n = 61), and PD + RBD + OSA (n = 31). Minimum oxygen saturation (SaO) during whole sleep and in REM sleep was higher in PD + RBD + OSA patients than that in PD + OSA patients. PD + RBD patients had worse Mini-Mental Status Examination and Montreal Cognitive Assessment (MoCA) scores than those in the PD group (P < 0.001), especially in visuospatial/executive, attention, and memory functions. The PD + OSA group performed worse than the PD group in the delayed recall domain. After adjusting for age, sex, body mass index, education, disease severity, and other sleep disorders, MoCA was negatively associated with OSA (β = -0.736, P = 0.043) and RBD (β = -2.575,P < 0.001). The severity of RBD (tonic/phasic electromyography activity) and OSA (apnea-hypopnea index/oxygen desaturation index/minimum SaO) were also associated with MoCA. The adjusted β values of RBD-related parameters were higher than that for OSA.</p><p><b>Conclusions</b>We found that RBD alleviated OSA severity; however, RBD and OSA together exacerbated PD cognitive impairment. Further studies are needed to evaluate whether OSA treatment can improve cognition in PD.</p>
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Aged , Female , Humans , Male , Middle Aged , Linear Models , Parkinson Disease , Pathology , Polysomnography , REM Sleep Behavior Disorder , Pathology , Sleep Apnea, Obstructive , Pathology , Sleep, REM , PhysiologyABSTRACT
<p><b>Objective</b>Rapid eye movement sleep behavior disorder (RBD) is characterized by dream enactment and loss of muscle atonia during rapid eye movement sleep. RBD is closely related to α-synucleinopathies including Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy. Many studies have investigated the markers of imaging and neurophysiological, genetic, cognitive, autonomic function of RBD and their predictive value for neurodegenerative diseases. This report reviewed the progress of these studies and discussed their limitations and future research directions.</p><p><b>Data Sources</b>Using the combined keywords: "RBD", "neurodegenerative disease", "Parkinson disease", and "magnetic resonance imaging", the PubMed/MEDLINE literature search was conducted up to January 1, 2018.</p><p><b>Study Selection</b>A total of 150 published articles were initially identified citations. Of the 150 articles, 92 articles were selected after further detailed review. This study referred to all the important English literature in full.</p><p><b>Results</b>Single-nucleotide polymorphisms in SCARB2 (rs6812193) and MAPT (rs12185268) were significantly associated with RBD. The olfactory loss, autonomic dysfunction, marked electroencephalogram slowing during both wakefulness and rapid eye movement sleep, and cognitive impairments were potential predictive markers for RBD conversion to neurodegenerative diseases. Traditional structural imaging studies reported relatively inconsistent results, whereas reduced functional connectivity between the left putamen and substantia nigra and dopamine transporter uptake demonstrated by functional imaging techniques were relatively consistent findings.</p><p><b>Conclusions</b>More longitudinal studies should be conducted to evaluate the predictive value of biomarkers of RBD. Moreover, because the glucose and dopamine metabolisms are not specific for assessing cognitive cognition, the molecular metabolism directly related to cognition should be investigated. There is a need for more treatment trials to determine the effectiveness of interventions of RBD on preventing the conversion to neurodegenerative diseases.</p>
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Humans , Biomarkers , Blood , Lysosome-Associated Membrane Glycoproteins , Genetics , Neurodegenerative Diseases , Blood , Genetics , Parkinson Disease , Blood , Genetics , Polymorphism, Single Nucleotide , Genetics , REM Sleep Behavior Disorder , Blood , Genetics , Receptors, Scavenger , Genetics , tau Proteins , GeneticsABSTRACT
Objective To investigate the morbidity of rapid eye movement sleep behavior disorder(RBD) in early Parkinson disease (PD)and its related factors. Methods One hundred twenty-five early PD patients were divided into RBD group (n=51)and non-RBD group (n=74),according to the complicated with RBD.We collected the clinical data and used univariate and multivariate logistic regression methods to analyze the risk factors for rapid eye movement sleep behavior disorder in early Parkinson disease. Results The incidence of RBD is 40.80% in early PD patients.Univariate analysis showed that the age, the motor phenotype (akinetic-rigid-type), modified Hoehn-Yahr(H-Y)grade, freezing, constipation and restless leg syndrome (RLS)were significantly higher in RBD group than in non-RBD group (P<0.05). Multivariate logistic regression revealed that constipation ( P=0.001,95% CI:1.980~12.253,OR=12.912)and RLS (P=0.014, 95% CI: 1.322~12.015, OR=6.378 ) were independent influencing factors for RBD in early PD patients. Conclusion Early PD patients with constipation or RLS are prone to RBD.
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Objective To investigate clinical features of tremors in PD patients with rapid eye movement sleep behavior disorder (RBD) and their response to medication. Methods PD patients were divided into PD with clinically possible (cp) RBD (PD+cpRBD) and PD without cpRBD (PD-cpRBD) according to RBDSQ scale. Hoehn & Yahr (H-Y) grade ,UPDRS-Ⅲ scale and MDS-UPDRS tremor scale were used to evaluate the motor function of the patients and amplitude of rest, kinetic and postural tremors of the first affected limbs. The re-sults were compared between these two groups including the features of the general information and tremor as well as the maximal improvement rate of UPDRS-Ⅲ and MDS-UPDRS tremor scores to acute levodopa chal-lenge test. Results A total of 42 PD patients with tremors were enrolled in this study, including 19 patients in PD+cpRBD group and 23 patients in PD-cpRBD group. There was no significant difference in sex, age, age of onset, duration of disease, UPDRS-Ⅲ score and H-Y grade between two groups (P>0.05). The tremor scores of the "off" state were significantly higher in PD+cpRBD group than in PD-cpRBD group (t=2.379,P=0.022). Compared with PD-cpRBD group, the progression of tremor from one side to other side was faster(u=-2.133,P=0.033)and the amplitude scores of rest and kinetic tremors were higher in PD+cpRBD group (rest tremor :u=-2.956,P=0.003;kinetic tremor:u=-2.657,P=0.008). The maximal improvement rate of UPDRS-Ⅲ and tremor score was significantly higher in PD-cpRBD group than in PD+cpRBD group after taking levodopa/ benserazide (200/50 mg) (UPDRS-Ⅲ:u=-3.134,P=0.002;tremor score: t=-3.189,P=0.003). Conclusion The present study has demonstrated severe tremors especially rest and kinetic tremors and poor response to levodopa in PD patients with cpRBD.
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Objective To explore the rapid eye movement (REM) sleep characteristics of different episode types of depression and post-stroke depression (PSD) patients and provide support for clinical diagnosis,treatment and prognosis.Methods Patients with single-episode depression (group A,n =22),patients with recurrent depression (≥ 2 episodes,group B,n=26) and patients with PSD (group C,n=19)were included from Henan Provincial Mental Hospital.20 healthy volunteers were assigned to control group.Participants in the 4 groups were performed polysomnographic recordings (PSG) from 9 PM to 6 AM before treatment.The 3 patients groups were performed the second PSG recordings and HAMD score at the end of 6 week SSRIs treatment.The REM indexes of 4 groups were compared and analyzed.Results First PSG detection showed that REM sleep latencies (RL) were shorter in group A and B (A:(65.57±18.29) min,B:(66.32±15.46) min) than that in group C ((79.17±20.18) min) and control group((87.24±16.55)min);REM activity (RA) (A:(99.82±25.71) u,B:(104.70±28.23) u)and REM density (RD) (A:(81.06± 19.35)％,B:(86.61±23.83) ％) were increased more significantly in group A and B than those in control group ((79.61 ± 18.40) u;(68.11 ± 17.54) ％);REM sleep time (RT) were decreased more signifi-cantly in group C ((51.66±22.26) min) than that in group A((71.43±20.70) min),group B((74.81±17.52) min) and control group ((70.46±16.35) min)(P＜0.05).After treatment,REM sleep latency was prolonged in group A ((65.57±18.29) min vs (81.71±21.62) min),and REM activity was decreased in group A((99.82±25.71) u vs (83.58±27.19) u),the difference was statistically significant (P＜0.05).REMdensity was decreased,but the difference was not statistically significant (P＞0.05).There was no significant difference in the indexes of REM in group C;RT was prolonged ((51.66± 22.26) min vs (68.37 ± 20.16)min) in group C,the difference was statistically significant (P＜0.05).Conclusion Most of depression patients with different episode types have REM disinhibition phenomenon.RD increase may be REM characteristic type of depression patient.Sleep disorders of PSD patients are mainly poor sleep process and sleep continuity and have no characteristics of REM sleep disorder of depression ones.
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Objective To explore the rapid eye movement (REM) sleep characteristics of different episode types of depression and post-stroke depression (PSD) patients and provide support for clinical diagnosis,treatment and prognosis.Methods Patients with single-episode depression (group A,n =22),patients with recurrent depression (≥ 2 episodes,group B,n=26) and patients with PSD (group C,n=19)were included from Henan Provincial Mental Hospital.20 healthy volunteers were assigned to control group.Participants in the 4 groups were performed polysomnographic recordings (PSG) from 9 PM to 6 AM before treatment.The 3 patients groups were performed the second PSG recordings and HAMD score at the end of 6 week SSRIs treatment.The REM indexes of 4 groups were compared and analyzed.Results First PSG detection showed that REM sleep latencies (RL) were shorter in group A and B (A:(65.57±18.29) min,B:(66.32±15.46) min) than that in group C ((79.17±20.18) min) and control group((87.24±16.55)min);REM activity (RA) (A:(99.82±25.71) u,B:(104.70±28.23) u)and REM density (RD) (A:(81.06± 19.35)％,B:(86.61±23.83) ％) were increased more significantly in group A and B than those in control group ((79.61 ± 18.40) u;(68.11 ± 17.54) ％);REM sleep time (RT) were decreased more signifi-cantly in group C ((51.66±22.26) min) than that in group A((71.43±20.70) min),group B((74.81±17.52) min) and control group ((70.46±16.35) min)(P＜0.05).After treatment,REM sleep latency was prolonged in group A ((65.57±18.29) min vs (81.71±21.62) min),and REM activity was decreased in group A((99.82±25.71) u vs (83.58±27.19) u),the difference was statistically significant (P＜0.05).REMdensity was decreased,but the difference was not statistically significant (P＞0.05).There was no significant difference in the indexes of REM in group C;RT was prolonged ((51.66± 22.26) min vs (68.37 ± 20.16)min) in group C,the difference was statistically significant (P＜0.05).Conclusion Most of depression patients with different episode types have REM disinhibition phenomenon.RD increase may be REM characteristic type of depression patient.Sleep disorders of PSD patients are mainly poor sleep process and sleep continuity and have no characteristics of REM sleep disorder of depression ones.
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OBJECTIVE: Rapid eye movement sleep behavior disorder (RBD) is associated with α-synucleinopathies, such as Parkinson's disease (PD). We aimed to assess the differences in the clinical characteristics of PD with and without RBD. METHODS: Forty-two patients previously diagnosed with PD were evaluated for clinical history, motor and cognitive functioning using the Unified Parkinson's Disease Rating Scale (UPDRS) and Mini-Mental State Examination (MMSE), autonomic symptoms, sleep characteristics using the Pittsburg Sleep Quality Index (PSQI), and the presence of RBD using the Korean version of the RBD screening questionnaire (RBDSQ). The prevalence of RBD and the patients' demographic features were evaluated. The patients were classified into two groups, PD with RBD and PD without RBD, based on the RBDSQ scores. The motor and cognitive functions, as well as other clinical features of the two groups were compared. RESULTS: A total of 42 PD patients were enrolled. Eighteen patients were classified as PD with RBD. Compared to PD without RBD, PD with RBD showed higher scores of rigidity in the UPDRS subscale. Regarding sleep problems, PD with RBD revealed higher sleep disturbance, lower sleep efficiency, and lower overall sleep quality in the PSQI. There was no difference in cognitive dysfunction between the two groups according to the Korean version of the MMSE. CONCLUSIONS: PD with RBD was associated with poorer sleep and motor symptoms. Therefore, RBD symptoms in PD are possibly poor prognostic markers.
Subject(s)
Humans , Cognition , Mass Screening , Parkinson Disease , Prevalence , REM Sleep Behavior Disorder , Sleep, REMABSTRACT
Poria cocos is a well-known traditional Chinese traditional medicine (TCM) that grows around roots of pine trees in China, Korea, Japan, and North America. Poria cocos has been used in Asian countries to treat insomnia as either a single herb or part of an herbal formula. In a previous experiment, pachymic acid (PA), an active constituent of Poria cocos ethanol extract (PCE), increased pentobarbital-induced sleeping behaviors. The aim of this experiment was to evaluate whether or not PCE and PA modulate sleep architectures in rats as well as whether or not their effects are mediated through GABA(A)-ergic transmission. PCE and PA were orally administered to individual rats 7 days after surgical implantation of a transmitter, and sleep architectures were recorded by Telemetric Cortical encephalogram (EEG) upon oral administration of test drugs. PCE and PA increased total sleep time and non-rapid eye movement (NREM) sleep as well as reduced numbers of sleep/wake cycles recorded by EEG. Furthermore, PCE increased intracellular chloride levels, GAD65/67 protein levels, and alpha-, beta-, and gamma-subunits of GABA(A) receptors in primary cultured hypothalamic neuronal cells. These data suggest that PCE modulates sleep architectures via activation of GABA(A)-ergic systems. Further, as PA is an active component of PCE, they may have the same pharmacological effects.
Subject(s)
Animals , Humans , Rats , Administration, Oral , Asian People , China , Cocos , Electroencephalography , Ethanol , Eye Movements , Glutamate Decarboxylase , Japan , Korea , Medicine, Chinese Traditional , Neurons , North America , Pinus , Poria , Receptors, GABA-A , Sleep Initiation and Maintenance DisordersABSTRACT
Objective To describe characteristics of REM sleep behavior disorder in Wilson’s disease. Method Questionnaire-based interviews (patients and relatives), neurological examinations, two-week prospective dream-diary, video-polysomnography, transcranial sonography, MRI. Results Four Wilson’s disease cases with REM sleep behavior disorder were described; three had REM sleep behavior disorder as initial symptom. All showed mesencephalic tegmental/tectal sonographic hyperechogenicities and two presented ponto-mesencephalic tegmental MRI hyperintensities. Conclusion This first description of REM sleep behavior disorder in Wilson’s disease in literature documents REM sleep behavior disorder as a possible presenting symptom of Wilson’s disease and adds further evidence to the parallelism of Parkinson’s disease and Wilson’s disease in phenotype and brainstem topography, which ought to be further studied. REM sleep behavior disorder has prognostic relevance for neurodegeneration in α-synucleinopathies. In Wilson’s disease, usefulness of early diagnosis and treatment are already well established. REM sleep behavior disorder in Wilson’s disease offers a possible theoretical model for potential early treatment in this extrapyramidal and brainstem paradigm syndrome, previewing the possibility of neuroprotective treatment for REM sleep behavior disorder in “pre-clinical” Parkinson’s disease. .
Objetivo Descrever características do transtorno comportamental do sono REM (TCSR) na doença de Wilson (DW). Método Aplicação de entrevistas, vídeo-polissonografia, sonografia transcraniana (STC), ressonância magnética (RM), diário de sonhos. Resultados Descrevemos quatro casos de DW com TCSR. Três apresentaram o TCSR como primeira manifestação. Todos mostraram hiperecogenicidades mesencefálicas na STC, dois apresentaram hiperintensidades ponto-mesencefálicas na RM. Conclusão Esta é a primeira descrição do TCSR na DW. Relatamos o TCSR como um sintoma inicial da DW. Acrescentamos prova para o paralelismo entre a doença de Parkinson e DW, com relação aos fenótipos e localização das lesões cerebrais. Nas alfa-sinucleinopatias, o TCSR tem relevância prognóstica quanto à neurodegeneração. Na DW, já conhecemos a importância de diagnóstico e tratamento precoces. O TCSR na DW oferece um modelo para antecipar o tratamento desta síndrome de acometimento dos núcleos basais e tronco, vislumbrando a possibilidade de tratamento neuroprotetor para a fase “pré-clínica” da DP. .
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Adult , Female , Humans , Male , Young Adult , Hepatolenticular Degeneration/physiopathology , REM Sleep Behavior Disorder/physiopathology , Early Diagnosis , Hepatolenticular Degeneration/drug therapy , Hepatolenticular Degeneration/pathology , Magnetic Resonance Imaging , Neurologic Examination , Neurodegenerative Diseases/physiopathology , Polysomnography , REM Sleep Behavior Disorder/drug therapy , REM Sleep Behavior Disorder/pathology , Surveys and Questionnaires , Ultrasonography, Doppler, TranscranialABSTRACT
Objective To explore ihe physiological changes of the late-onset depressive(LOD) persons during sleep.Methods 15 cases of LOD patients formed a group and 10 healthy aging persons formed a control group.Hamilton Depression Scale (HAMD) was used to score the severity of depression and polysomnographic recorders were used to monitor the whole night long.The subjective feelings of the sleep and the daytime mental status were assessed in the morning.Results Compared with the controlde group, the LOD patients obviously possessed a disordered sleeping process: sleep efficiency was lower( ( 59.20 ± 2.90 ) %, ( 77.09 ± 1.55 ) %, P ＜0.01 ); their sleep latency was longer( (54.00 ± 4.97 ), ( 24.00 ± 2.91 ), P ＜ 0.01 ); the numbers of rapid eye movement(REM) sleep phase and rapid eye movement latency(REML) were strikingly different(P＜0.01 ).Compad with the control group, the LOD patients' awakening time and percent were significantly increased.Not only were the time and percentage of S2 sleep phase much higher, but the time of slow wave sleep was shorter.Besides,REM sleep activity, its density, and its intensity were raised (P ＜ 0.05 ).Conclusion There is a disturbance of the objective physiological indexes happening among the LOD patients.The increase of S2 sleeping time and percentage and the disinhibition of REM sleep can be used as the diagnosis indexes of LOD patients' specificity.