Assessing gray matter volume in patients with idiopathic rapid eye movement sleep behavior disorder

Idiopathic rapid eye movement sleep behavior disorder(iRBD) is often a precursor to neurodegenerative disease. However, voxel-based morphological studies evaluating structural abnormalities in the brains of iRBD patients are relatively rare. This study aimed to explore cerebral structural alterations using magnetic resonance imaging and to determine their association with clinical parameters in iRBD patients. Brain structural T1-weighted MRI scans were acquired from 19 polysomnogram-confirmed iRBD patients(male:female 16:3; mean age 66.6 ± 7.0 years) and 20 age-matched healthy controls(male:female 5:15; mean age 63.7 ± 5.9 years). Gray matter volume(GMV) data were analyzed based on Statistical Parametric Mapping 8, using a voxel-based morphometry method and two-sample t-test and multiple regression analysis. Compared with controls, iRBD patients had increased GMV in the middle temporal gyrus and cerebellar posterior lobe, but decreased GMV in the Rolandic operculum, postcentral gyrus, insular lobe, cingulate gyrus, precuneus, rectus gyrus, and superior frontal gyrus. iRBD duration was positively correlated with GMV in the precuneus, cuneus, superior parietal gyrus, postcentral gyrus, posterior cingulate gyrus, hippocampus, lingual gyrus, middle occipital gyrus, middle temporal gyrus, and cerebellum posterior lobe. Furthermore, phasic chin electromyographic activity was positively correlated with GMV in the hippocampus, precuneus, fusiform gyrus, precentral gyrus, superior frontal gyrus, cuneus, inferior parietal lobule, angular gyrus, superior parietal gyrus, paracentral lobule, and cerebellar posterior lobe. There were no significant negative correlations of brain GMV with disease duration or electromyographic activity in iRBD patients. These findings expand the spectrum of known gray matter modifications in iRBD patients and provide evidence of a correlation between brain dysfunction and clinical manifestations in such patients. The protocol was approved by the Ethics Committee of Huashan Hospital(approval No. KY2013-336) on January 6, 2014. This trial was registered in the ISRCTN registry(ISRCTN18238599).

Chemogenetic activation of sublaterodorsal tegmental glutamatergic neurons alleviates rapid eye movement sleep behavior disorder symptoms in a chronic rat model of Parkinson disease

Rapid eye movement(REM)sleep behavior disorder(RBD)is a parasomnia that is featured by elevated motor behaviors and dream enactments during REM sleep.Clinical observations show that RBD bears significant relevance with several synucleinopathies such as Lewy body dementia and Parkinson disease(PD),and often develops prior to their diagnosis.Being a potential biomarker of PD,investigating the relationship of RBD symptoms and their emergence in developing PD would provide insight intoits pathogenesis.Here,in a chronic model of PD,rats with daily rotenone treatment exhibited key RBD features,including elevated sleep muscle tone,sleep fragmentation and EEG slowing at different time points.Based on detectedearly alpha synuclein aggregation and neural apoptosis in the sublaterodorsal tegmental nucleus(SLD),an area known to promote REM sleep and maintain sleep muscle atonia,the possible involvement of SLD glutamatergic neurons was interrogated.Via chemogenetic activation of SLD glutamatergic neurons,key RBD symptoms and EEG slowing in REM sleep were alleviated.These results are consistent with a progressive degeneration in REM sleep promoting pathways.Our findings provide a foundation for further studies into RBD and its relationship to neurodegenerative diseases.

Effect of Rapid Eye Movement Sleep Behavior Disorder on Obstructive Sleep Apnea Severity and Cognition of Parkinson＇s Disease Patients

Background：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.Methods：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.Results：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 （SaO2） 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 SaO2） were also associated with MoCA. The adjusted β values of RBD-related parameters were higher than that for OSA.Conclusions：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.

Rapid Eye Movement Sleep Behavior Disorder Symptoms Correlate with Domains of Cognitive Impairment in Parkinson＆#39;s Disease

Background： Rapid eye movement （REM） sleep behavior disorder （RBD） may be a risk factor for cognitive impairment in patients with Parkinson＆#39;s disease （PD）.However, little is known regarding the relation between the severity of RBD and the different domains of cognitive impairment.The aim of this study was： （1） to investigate the domains of cognitive impairment in patients with PD and RBD, and （2） to explore risk factors for PD-mild cognitive impairment （PD-MCI） and the relationship between RBD severity and impairment in different cognitive domains in PD.Methods： The participants were grouped as follows： PD without RBD （PD-RBD;n =42）, PD with RBD （PD ＋ RBD;n =32）, idiopathic RBD （iRBD;n =15）, and healthy controls （HCs;n =36）.All participants completed a battery of neuropsychological assessment of attention and working memory, executive function, language, memory, and visuospatial function.The information of basic demographics, diseases and medication history, and motor and nonmotor manifestations was obtained and compared between PD-RBD and PD ＋ RBD groups.Particular attention was paid to the severity of RBD assessed by the RBD Questionnaire-Hong Kong （RBDQ-HK） and the RBD Screening Questionnaire （RBDSQ）, then we further examined associations between the severity of RBD symptoms and cognitive levels via correlation analysis.Results： Compared to PD-RBD subjects, PD ＋ RBD patients were more likely to have olfactory dysfunction and their Epworth Sleepiness Scale scores were higher （P 〈 0.05）.During neuropsychological testing, PD ＋ RBD patients performed worse than PD-RBD patients, including delayed memory function, especially.The MCI rates were 33%, 63%, 33%, and 8% for PD-RBD, PD ＋ RBD, iRBD, and HC groups, respectively.RBD was an important factor for the PD-MCI variance （odds ratio =5.204, P =0.018）.During correlation analysis, higher RBDSQ and RBDQ-HK scores were significantly associated with poorer performance on the Trail Making Test-B （errors） and Auditory Verbal Learning Test （delayed recall） and higher RBD-HK scores were also associated with Rey-Osterrieth complex figure （copy） results.Conclusions： When PD-RBD and PD ＋ RBD patients have equivalent motor symptoms, PD ＋ RBD patients still have more olfactory dysfunction and worse daytime somnolence.RBD is an important risk factor for MCI, including delayed memory.Deficits in executive function, verbal delayed memory, and visuospatial function were consistently associated with more severe RBD symptoms.

Clinical features of Parkinson’s disease with and without rapid eye movement sleep behavior disorder

Background:Rapid eye movement sleep behavior disorder(RBD)and Parkinson’s disease(PD)are two distinct clinical diseases but they share some common pathological and anatomical characteristics.This study aims to confirm the clinical features of RBD in Chinese PD patients.Methods:One hundred fifty PD patients were enrolled from the Parkinson`s disease and Movement Disorders Center in Department of Neurology,Shanghai General Hospital from January 2013 to August 2014.This study examined PD patients with or without RBD as determined by the REM Sleep Behavior Disorder Screening Questionnaire(RBDSQ),assessed motor subtype by Unified PD Rating Scale(UPDRS)III at“on”state,and compared the sub-scale scores representing tremor,rigidity,appendicular and axial.Investigators also assessed the Hamilton Anxiety Scale(HAMA),Hamilton Depression Scale(HAMD),Mini-Mental State Examination(MMSE),Clinical Dementia Rating(CDR),and Parkinson’s disease Sleep Scale(PDSS).Results:One hundred fourty one PD patients entered the final study.30(21.28%)PD patients had probable RBD(pRBD)diagnosed with a RBDSQ score of 6 or above.There were no significant differences for age,including age of PD onset and PD duration,gender,smoking status,alcohol or coffee use,presence of anosmia or freezing,UPDRS III,and H-Y stages between the pRBD+and pRBD−groups.pRBD+group had lower MMSE scores,higher PDSS scores,and pRBD+PD patients had more prominent proportion in anxiety,depression,constipation,hallucination and a greater prevalence of orthostatic hypotension.Conclusion:pRBD+PD patients exhibited greater changes in non-motor symptoms.However,there was no increase in motor deficits.

CSF Aβ1-42 level is associated with cognitive decline in early Parkinson’s disease with rapid eye movement sleep behavior disorder

Background:Rapid eye movement sleep behavior disorder(RBD)is associated with cognitive decline in early Parkinson’s disease(PD).However,the underlyling basis for this association remains unclear.Methods:Parkinson’s Progression Marker’s Initiative(PPMI)subjects underwent baseline RBD testing with RBD sleep questionnaire(RBDSQ).Serial assessments included measures of motor symptoms,non-motor symptoms(NMS),neuropsychological assessment,blood and cerebrospinal fluid(CSF)biomarkers.Up to three years follow-up data were included.We stratified early PD subjects into PD with RBD(RBDSQ score>5)and PD without RBD groups.Then,we evaluated baseline biomarkers in each group as a predictor of cognitive decline using Montreal Cognitive Assessment(MoCA)score changes over three years in regression models.Results:Four hundred twenty-three PD subjects were enrolled at baseline,and a total of 350 PD subjects had completed 3 years of study follow-up with completely serial assessments.We found that at baseline,only CSF β-amyloid 1–42(Aβ1–42)was significantly lower in PD subjects with RBD.On three years follow-up analysis,PD subjects with RBD were more likely to develop incident mild cognitive impairment(MCI)and presented greater cognitive decline in MoCA score.Lower baseline CSF Aβ1–42 predicted cognitive decline over 3 years only in PD subjects with RBD(β=−0.03,P=0.003).A significant interaction between Aβ1–42 and the 2 groups confirmed that this effect was indeed higher in PD with RBD than the other individual(β=−2.85,P=0.014).Conclusion:These findings indicate that CSF Aβ1–42 level is associated with global cognitive decline in early PD with RBD.The addition of CSF Aβ1–42 to RBD testing increase the likelihood of identifying those at high risk for cognitive decline in early PD.

Comparison Study of Polysomnographic Features in Multiple System Atrophy-cerebellar Types Combined with and without Rapid Eye Movement Sleep Behavior Disorder

Background： The brain stem is found to be impaired in multiple system atrophy-ccrcbellar types （MSA-C）. Rapid eye movement （REM） sleep behavior disorder （RBD） is reported as a marker of progressive brain stem dysfunction. Few systematic studies about the sleep disturbances in MSA-C patients combined with or without RBD were reported. This study aimed to explore the polysomnographic （PSG） features of sleep disturbances between MSA-C patients with and without RBD. Methods： Totally, 46 MSA-C patients （23 with RBD, and 23 without RBD） were enrolled in this study. All patients underwent a structured interview for their demographic data, history of sleep pattern, and movement disorders; and then, overnight video-PSG was performed in each patient. All the records were evaluated by specialists at the Sleep Medicine Clinic for RBD and the Movement Disorder Clinic for MSA-C. The Student＇s t-test, Mann-Whitney U-test for continuous variables, and the Chi-square test for categorical variables were used in this study. Results： MSA-C patients with RBD had younger visiting age （52.6 ± 7.4 vs. 56.7 ± 6.0 years, P = 0.046） and shorter duration of the disease （12.0 [12.0, 24.0] vs. 24.0 [14.0, 36.0] months, P 0.009） than MSA-C patients without RBD. MSA-C with RBD had shorter REM sleep latency （111.7 ± 48.2 vs. 157.0 ± 68.8 rain, P = 0.042）, higher percentage of REM sleep （14.9% ±4.0% vs. 10.0% ± 3.2%, P = 0.019）, and lower Stage 1 （9.5% ±7.2% vs. 15.9% ±8.0%, P= 0.027） than MSA-C without RBD. Moreover, MSA-C patients with RBD had more decreased sleep efficiency （52.4% ±12.6% vs. 65.8% ±15.9%, P = 0.029） than that without RBD. Conclusions： In addition to the RBD, MSA-C patients with RBD had other more severe sleep disturbances than those without RBD. The sleep disorders of MSA patients might be associated with the progress of the disease.

Relationships between Rapid Eye Movement Sleep Behavior Disorder and Neurodegenerative Diseases： Clinical Assessments, Biomarkers, and Treatment

Objective： 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. Data Sources： 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. Study Selection： 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. Results： 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. Conclusions： 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 treatnaent trials to determine the effectiveness of interventions of RBD on preventing the conversion to neurodegenerative diseases.

Clinical Significance of REM Sleep Behavior Disorders and Other Non-motor Symptoms of Parkinsonism

Rapid eye movement sleep behavior disorder （RBD） is one of the most common non-motor symptoms of parkinsonism, and it may serve as a prodromal marker of neurodegenerative disease. The mechanism underlying RBD is unclear. Several prospective studies have reported that specific non-motor symptoms predict a conversion risk of developing a neurodegenerative disease, including olfactory dysfunction, abnormal color vision, autonomic dysfunction, excessive daytime sleepiness, depression, and cognitive impairment. Parkinson＇s disease （PD） with RBD exhibits clinical heterogeneity with respect to motor and non-motor symptoms compared with PD without RBD. In this review, we describe the main clinical and pathogenic features of RBD, focusing on its association with other non-motor symptoms of parkinsonism.

Longitudinal evolution of cortical thickness signature reflecting Lewy body dementia in isolated REM sleep behavior disorder:a prospective cohort study

Background The isolated rapid-eye-movement sleep behavior disorder(iRBD)is a prodromal condition of Lewy body disease including Parkinson’s disease and dementia with Lewy bodies(DLB).We aim to investigate the longitudinal evolution of DLB-related cortical thickness signature in a prospective iRBD cohort and evaluate the possible predictive value of the cortical signature index in predicting dementia-first phenoconversion in individuals with iRBD.Methods We enrolled 22 DLB patients,44 healthy controls,and 50 video polysomnography-proven iRBD patients.Participants underwent 3-T magnetic resonance imaging(MRI)and clinical/neuropsychological evaluations.We characterized DLB-related whole-brain cortical thickness spatial covariance pattern(DLB-pattern)using scaled subprofile model of principal components analysis that best differentiated DLB patients from age-matched controls.We analyzed clinical and neuropsychological correlates of the DLB-pattern expression scores and the mean values of the whole-brain cortical thickness in DLB and iRBD patients.With repeated MRI data during the follow-up in our prospective iRBD cohort,we investigated the longitudinal evolution of the cortical thickness signature toward Lewy body dementia.Finally,we analyzed the potential predictive value of cortical thickness signature as a biomarker of phenoconversion in iRBD cohort.Results The DLB-pattern was characterized by thinning of the temporal,orbitofrontal,and insular cortices and relative preservation of the precentral and inferior parietal cortices.The DLB-pattern expression scores correlated with attentional and frontal executive dysfunction(Trail Making Test-A and B:R=−0.55,P=0.024 and R=−0.56,P=0.036,respectively)as well as visuospatial impairment(Rey-figure copy test:R=−0.54,P=0.0047).The longitudinal trajectory of DLB-pattern revealed an increasing pattern above the cut-off in the dementia-first phenoconverters(Pearson’s correlation,R=0.74,P=6.8×10−4)but no significant change in parkinsonism-first phenoconverters(R=0.0063,P=0.98).The mean value of the whole-brain cortical thickness predicted phenoconversion in iRBD patients with hazard ratio of 9.33[1.16-74.12].The increase in DLB-pattern expression score discriminated dementia-first from parkinsonism-first phenoconversions with 88.2%accuracy.Conclusion Cortical thickness signature can effectively reflect the longitudinal evolution of Lewy body dementia in the iRBD population.Replication studies would further validate the utility of this imaging marker in iRBD.

Sleep Disturbance in Parkinson’s Disease Varies with Age of Onset and Family History

Introduction: Parkinson’s disease (PD) is a progressive neurodegenerative disease more common in those over the age of 60. PD is classically characterized by motor features, although patients may also experience non-motor symptoms. Sleep disturbances, such as rapid eye movement (REM) behavior disorder (RBD), are common in patients with PD and may precede onset of PD. Methods: Data was collected on patients with PD (358 subjects)in a movement disorders clinic at a safety net hospital. In this retrospective database analysis, the association of PD complications with age of onset was evaluated using chi-square tests and logistic regression. Results: Of the PD complications analyzed, there was a significant difference in sleep disturbances by age. Among the 358 PD patients, 120 individuals (33.5%) had information regarding the presence or absence of sleep disturbances. There was a significant difference between the early (onset < 50) and later onset (≥50) groups (p = 0.03) with the odds of having a sleep disorder for the early group 1.6 times that of the late group. Those subjects with siblings who also had PD had 2.0 times the odds of having a sleep disorder compared those without (p = 0.02). Conclusion: Non-motor symptoms such as sleep disorders are a useful predictor of early onset PD. Genetic components of PD impact both motor and non-motor aspects of the disease.

帕金森病伴睡眠障碍的研究进展

帕金森病(PD)是一种与运动和非运动症状相关的大脑退行性疾病,与环境、遗传、神经系统老化等多种因素有关。近年的调查研究显示,中国PD平均患病年龄60岁,在65岁以上人群中,每10万人约1700名患者。睡眠障碍是PD的非运动症状之一,临床表现包括失眠、白天过度嗜睡、不宁腿综合征、快速眼动期睡眠行为障碍以及睡眠呼吸障碍等多种类型。由于存在个体差异,PD伴睡眠障碍疾病治疗过程中应在医生指导下选择最适合患者个体的药物。本文对PD睡眠障碍发病机制和常用药物治疗方案进行综述,希望能够为今后PD伴睡眠障碍的治疗提供新的思路。

伴和不伴快速眼动睡眠行为障碍帕金森病患者自发脑活动的静息态功能磁共振成像研究

目的快速眼动睡眠行为障碍(rapid eye movement sleep behavior disorder,RBD)是帕金森病(Parkinson's disease,PD)常见的非运动症状且是重要预后因素。本研究通过静息态功能磁共振成像,利用度中心度(degreecentrality,DC)和低频振幅(amplitudes of low-frequency fluctuation,ALFF)分析PD伴RBD和不伴有RBD患者组以及健康对照组三组间DC值和ALFF值,探索PD伴RBD患者脑功能活动特征及RBD特异性脑区,探究RBD发生的病理机制。材料与方法招募20例伴有RBD的PD患者(PD-RBD组)、40例无RBD的PD患者(PD-nonRBD组)和44例年龄性别匹配的健康对照(健康对照组),三组被试均接受磁共振扫描。利用静息态数据计算DC值和ALFF值,探测脑功能特征。结果方差分析结果显示三组间DC值主效应脑区为右侧中央前回、颞上回、小脑、额中回(P<0.05,FDR校正);ALFF值主效应脑区为左侧海马旁回、楔叶、舌回(P<0.05,FDR校正)。进一步分析发现相比于PD-nonRBD组,PD-RBD患者表现为右侧额中回DC值升高(t=4.02;P=0.007,FDR校正);左侧楔前叶DC值降低(t=5.30;P=0.009,FDR校正)。相比于健康对照组,PD-RBD患者表现为左侧额上回、小脑、右侧颞上回、左侧颞中回、额中回的DC值升高(P<0.05,FDR校正);左侧中央前回、颞上回和颞中回的DC值降低(P<0.05,FDR校正);右侧楔叶ALFF值降低(P<0.05,FDR校正)。结论PD-RBD在DC和ALFF上有独特的影像学特征,特别是右侧额中回、左侧楔前叶的功能异常可能与PD患者RBD的发生密切相关。

重复经颅磁刺激治疗帕金森病伴快速眼动睡眠行为障碍观察

目的探讨重复经颅磁刺激对帕金森病伴快速眼动睡眠行为障碍患者实施治疗的可行性与安全性。方法回顾性分析福州市第二医院2021年3月—2023年3月收治的帕金森病伴快速眼动睡眠行为障碍患者病例资料,查阅并筛选出100例帕金森病伴快速眼动睡眠行为障碍患者完整病例,根据治疗方案分为2组,各50例。参照组采取药物治疗,研究组则在参照组治疗基础上配合重复经颅磁刺激治疗。比较2组治疗效果。结果2组患者治疗后的总睡眠时间(total sleep time,TST)、睡眠效率(sleep efficiency,SE)、快速眼动睡眠时间(rapid eye movement sleep,REMS)比治疗前更高,且研究组治疗后的指标[(360.45±25.68)min、(76.15±5.15)%、(12.85±4.32)min]均高于参照组[(317.85±23.12)min、(68.76±4.31)%、(8.05±1.65)min];而睡眠潜伏期(sleeplatency,SL)、醒觉指数(arousalindex,AI)则要低于治疗前,且研究组治疗后的指标[(17.12±3.45)min、(24.05±2.48)次/h]低于参照组[(24.18±4.36)min、(35.36±3.12)次/h],差异有统计学意义(P<0.05)。治疗后,2组的爱泼沃斯嗜睡量表(Epworth sleeping scale,ESS)评分要低于治疗前,且研究组治疗后评分[(6.01±2.02)分]低于参照组[(8.12±2.05)分],而蒙特利尔认知评估量表(Montreal cognitive assess-ment scale,MoCA)评分、PD睡眠量表(PDsleepscale,PDSS)评分高于治疗前,且研究组治疗后的分数[(25.38±2.76)分、(119.85±11.05)分]明显高出参照组[(22.38±2.13)分、(113.15±10.35)分],差异有统计学意义(P<0.05)。2组不良反应发生率比较,差异无统计学意义(P>0.05)。结论对于帕金森病伴快速眼动睡眠行为障碍采取重复经颅磁刺激治疗,可取得良好治疗效果,对于患者的睡眠障碍改善、认知功能改善有积极作用,且不会增加患者的不良反应发生率,具有较高的安全性。

伴快速眼动期睡眠行为障碍帕金森病患者的睡眠结构及其与认知功能、抑郁状态、运动功能的相关性

目的探讨伴快速眼动期睡眠行为障碍(RBD)的帕金森病(PD)患者的睡眠结构及其与认知功能、抑郁状态、运动功能的相关性。方法选取120例PD患者为研究对象,根据是否合并RBD分为PD+RBD组(n=45)和PD组(n=75)。记录2组睡眠结构情况;比较2组的蒙特利尔认知评估量表(MoCA)、汉密尔顿焦虑量表(HAMA)、汉密尔顿抑郁量表(HAMD)、统一帕金森病评价量表第3部分(UPDRS-Ⅲ)以及自主神经症状量表(SCOPA-AUT)评分。分析PD+RBD组患者睡眠结构与MoCA、HAMA、HAMD、UPDRS-Ⅲ、SCOPA-AUT评分的相关性。结果PD+RBD组的非快速眼动(NREM)1期占比、睡眠觉醒指数、睡眠中周期性肢体运动(PLMS)和呼吸暂停低通气指数(AHI)高于PD组,NREM 3期占比、快速眼动(REM)期睡眠占比、睡眠效率和最低血氧低于PD组,差异有统计学意义(P<0.05)。PD+RBD组的HAMA、HAMD、UPDRS-Ⅲ、SCOPA-AUT评分高于PD组,MoCA评分低于PD组,差异有统计学意义(P<0.05)。PD+RBD组NREM 1期睡眠占比、睡眠觉醒指数、PLMS、AHI与HAMA、HAMD、UPDRS-Ⅲ、SCOPA-AUT评分呈正相关,而与MoCA评分呈负相关(P<0.05);NREM 3期睡眠占比、REM期睡眠占比、睡眠效率、最低血氧与HAMA、HAMD、UPDRS-Ⅲ、SCOPA-AUT评分呈负相关,而与MoCA评分呈正相关(P<0.05)。结论伴有RBD的PD患者存在睡眠结构紊乱,并与认知功能、抑郁状态、运动功能及自主神经功能密切相关。

表现为多系统萎缩小脑型脊髓小脑性共济失调8型1例

报道1例表现为多系统萎缩小脑型的脊髓小脑性共济失调8型(spinocerebellar ataxia type 8,SCA8)患者。该患者为57岁男性,病程4年,以头晕、共济失调为首发症状,后出现自主神经功能障碍、快速眼动睡眠障碍等表现。神经系统查体提示自主神经功能障碍、眼球震颤、构音障碍、共济失调,颅脑核磁共振见脑干、小脑对称性萎缩及脑桥“十字征”。基因检测结果显示ATXN8OS的两个等位基因CTA/CTG重复次数异常增多,确诊为SCA8。治疗上予以改善共济失调、自主神经功能障碍等对症治疗后患者反应良好。SCA8为罕见的运动障碍性疾病,临床异质性高。本报道旨在提示临床医师,SCA8也可表现为自主神经功能障碍、共济失调、脑桥“十字征”等类似多系统萎缩小脑型的特点,临床工作中要避免误诊、漏诊。

帕金森病伴睡眠障碍患者脑结构及功能异常的神经影像学研究

在帕金森病(PD)领域,睡眠障碍被公认为是最常出现的非运动症状之一,其与该疾病运动性及非运动性症状的发展进程紧密相关。研究表明PD伴睡眠障碍(如快速眼动睡眠行为障碍)患者较不伴睡眠障碍患者疾病进展更快,且大多数睡眠障碍患者最终都会进展为PD。目前对于睡眠障碍与PD发病机制间的关联尚未充分阐明,因此及早发现PD合并睡眠障碍患者的异常结构及功能变化,对于延缓疾病进展及预防睡眠障碍向PD的转化具有重要价值。近年来,随着影像学技术的不断发展及其广泛应用,诸多神经影像学技术已广泛应用在PD伴非运动症状患者的研究中,如弥散张量成像、静息态功能磁共振成像、神经黑色素敏感成像、SPECT/PET及经颅超声等,它们在帕金森病的研究中扮演着关键角色,其在疾病早期诊断、监测及明确发病机制方面具有重要价值。本文就上述神经影像技术在帕金森病伴睡眠障碍患者的影像学研究进展予以综述,以更全面地理解PD伴睡眠障碍的病理生理机制,并指导临床诊断和治疗。

伴自主神经功能障碍的帕金森病患者的睡眠结构及其与快速眼动睡眠障碍的相关性

目的探讨伴发自主神经功能障碍的帕金森病(PD)患者的睡眠结构及其与快速眼动睡眠障碍(RBD)的关系。方法收集48例PD患者的一般资料。根据皮肤交感反应(SSR)检查,将患者分为SSR正常组及SSR障碍组。应用统一PD评定量表第三部分(UPDRS-Ⅲ)、Hoehn-Yahr(H-Y)分级、汉密尔顿焦虑量表(HAMA14)、汉密尔顿抑郁量表(HAMD24)、匹兹堡睡眠指数量表(PSQI)、MMSE、蒙特利尔认知评估量表(MoCA)、自主神经症状量表(SCOPA-AUT)评估患者的运动、非运动症状及自主神经功能;RBD筛查量表(RBDSQ)评定患者RBD症状;多导睡眠监测(PSG)记录睡眠参数。结果与SSR正常组比较,SSR障碍组病程显著延长,H-Y分级及HAMA14、HAMD24、PSQI、SCOPA-AUT、RBDSQ量表评分显著升高(P<0.05~0.01)。与SSR正常组相比,SSR障碍组患者睡眠效率及非快速眼动期(NREM)-Ⅱ期睡眠百分比显著下降,觉醒指数、NREM-Ⅰ期睡眠百分比、周期性腿动指数(PLMI)显著增高(P<0.05~0.01)。SSR障碍组周期性腿动和RBD比率均显著高于SSR正常组(χ^2=4.463,P=0.035;χ^2=8.889,P=0.003)。RBDSQ与SCOPA-AUT评分、NREM-Ⅰ期睡眠百分比、REM期睡眠百分比、呼吸暂停-低通气指数、PLMI和觉醒指数呈正相关(均P<0.01),与总睡眠时间、睡眠潜伏期、REM潜伏期、睡眠效率、NREM-Ⅱ期睡眠百分比、NREM-Ⅲ期睡眠百分比呈负相关(均P<0.01),与总觉醒时间无相关性。结论伴自主神经功能障碍的PD患者病程长,病情重,容易存在焦虑、抑郁情绪,客观存在睡眠结构紊乱,RBD发生率高。PD患者RBD的严重程度与自主神经功能障碍程度密切相关。

帕金森病伴发快速眼动期睡眠行为障碍的相关性研究

目的观察快速眼动期睡眠行为障碍(RBD)在帕金森病中的发生率、出现时间、电生理特点,探讨RBD与帕金森病之间的关系。方法通过对患者的既往睡眠状况调查以及多导睡眠监测(PSG).观察患者的睡眠障碍特征。(1)主观睡眠调查:帕金森病(PD)组患者60例,年龄匹配的健康对照组60例,询问睡眠史,了解RBD出现的比例及出现时间。(2)PSG:对120例受试者接受连续2夜的PSG监测,对出现RBD的帕金森病患者分析其PSG特点。结果 PD组合并RBD占75.0%(45/60),明显高于健康对照组的40.0%(24/60),其中RBD早于临床PD主症的患者比例是40.0%(18/45)。PSG检测结果发现:PD合并RBD最主要的PSG特点是:快速眼动睡眠(REM)期(快速眼动睡眠期)肌肉失弛缓和全身骨骼肌活动增多,与健康对照组比较,差异有统计学意义(t=23.2、20.6,P<0.01)。结论 PD患者伴发RBD率高,部分RBD先于经典运动症状出现,提示RBD可能为PD的早期表现。PSG特征可以作为PD伴发RBD的诊断指标之一。

帕金森病患者快速眼动睡眠行为障碍的临床特征

目的探讨帕金森病(PD)患者快速眼动睡眠行为障碍(RBD)的临床特征。方法连续收集2013年2月~2016年8月就诊于河北医科大学第一医院神经内科的61例PD患者,记录一般资料。对患者进行多导睡眠监测(PSG)和RBD筛查量表(RBDSQ)评估,根据结果将患者分为临床RBD组、亚临床RBD组和无RBD组。应用统一PD评定量表第三部分(UPDRSⅢ)、Hoehn-Yahr(H-Y)分级、汉密尔顿焦虑抑郁量表(HAMA14、HAMD24)、匹兹堡睡眠指数量表(PSQI)、MMSE、蒙特利尔认知评估量表(Mo CA)评估患者的运动及非运动症状,应用TCD检测患者黑质回声强度,对患者服用抗PD药物进行左旋多巴等效剂量(LDE)换算。结果最终入组56例患者,根据PSG和RBDSQ结果分为临床RBD组25例,亚临床RBD组22例,无RBD组9例。临床RBD组及亚临床RBD组病程明显短于无RBD组,两组患者所需的左旋多巴等效剂量(LDE)均多于无RBD组(均P<0.05)。临床RBD组的H-Y分级和PSQI评分均显著高于亚临床RBD组及无RBD组,亚临床RBD组的H-Y分级和PSQI评分显著高于无RBD组(均P<0.05)。临床RBD组TCD阳性检出率高于无RBD组(P<0.05)。RBDSQ评分与病程呈负相关,与H-Y分级、LDE、PSQI评分呈正相关(均P<0.05)。结论 PD患者RBD发生率高,伴RBD的患者病程短,RBD的严重程度与患者H-Y分级、LDE和总体睡眠质量显著相关。伴有临床RBD的PD患者黑质强回声的发生率高。