MoCA量表在评估帕金森病患者认知功能中的应用

目的 采用蒙特利尔认知评估量表(MoCA)分析帕金森病(PD)患者的认知功能损害的特点,并探讨MoCA在评估PD认知功能方面的应用价值.方法 采用MoCA对35例PD患者进行认知功能评估,并进行各认知域的分析.结果 (1)本组研究对象的MoCA评分为20.51±5.767,其中7例患者MoCA≤26分,占20.0%;(2)PD患者各认知域障碍的发生率不一致,依次为语言(34例,97.1%)、延迟记忆(32例,91.4%)、视空间与执行能力(30例,85.7%)、抽象思维(27例,77.1%)、注意(23例,68.6%)、命名(13例,37.1%)和定向力(12例,34.3%):(3)MoCA的各认知域与总分的相关系数都大于0.50,P＜0.01.结论 (1)MoCA是评估PD患者认知功能的高效快捷的工具;(2)PD患者常见的认知功能损害包括语言、延迟记忆、视空间与执行能力、抽象思维和注意,而命名和定向力相对损害较轻.     

蒙特利尔认知评价量表(中文版)在轻度认知损害诊断及进展过程中的作用

目的研究蒙特利尔认知评价量表(MoCA)中文版在轻度认知损害(MCI)诊断筛查中的作用,评价认知功能在疾病进展过程中的临床意义。方法对年龄、性别、文化程度构成无统计学差异的两组受试者(正常对照组29例、MCI组28例)进行MoCA和简易智能状态检查量表(MMSE)测试,以其总成绩及各单项成绩作为基线成绩,观察MoCA和MMSE在筛查MCI中的作用,并比较两种量表对筛查轻度认知损害的敏感性、特异性的差异。于初次筛查后12个月对两组受试者进行再次测试,并与基线成绩进行配对t检验,比较前后测试成绩间的差异及各单项成绩对预测疾病进展的作用。结果 MoCA和MMSE对鉴别正常老龄化和轻度认知损害均具有初步筛查作用,MoCA量表中的视空间执行功能(t=2.151,P=0.036)、抽象(t=2.787,P=0.009)、定向(t=3.162,P=0.003)、记忆(t=4.704,P=0.000)等单项测试成绩,两组间差异具有统计学意义;以26分为分界值,MoCA和MMSE诊断MCI的敏感度分别为89.29%和10.71%,特异度为82.76%和100%,MoCA诊断敏感性显著高于MMSE。MCI组患者在12个月后的随访测试中各项成绩均略有下降,其中MoCA总成绩(t=6.454,P=0.000)、视空间执行功能(t=5.610,P=0.000)、语言(t=4.954,P=0.000)测试成绩,复查前后差异有统计学意义。结论 MoCA对轻度认知损害的诊断敏感性高于MMSE,其中视空间执行功能、抽象、定向、记忆各单项测试成绩具有诊断价值;MoCA总评分、视空间执行功能、语言等项成绩复查后降低,对轻度认知损害向阿尔茨海默病转化具有提示作用。     

轻度认知功能障碍患者的神经心理学研究

目的 探讨轻度认知功能障碍(MCI)患者神经心理学的特点. 方法 对42例MCI患者和55例健康对照者进行多项神经心理学检查,包括简易精神状态检查量表(MMSE)、蒙特利尔认知评估量表(MoCA)、临床痴呆评定量表(CDR)、语言流畅性测验(RVR)、韦氏智力测验(WAIS-RC)[包括数字广度测验(DS)、积木测验(BD)、相似性测验]、韦氏记忆测验(WMS-R)(包括逻辑记忆、联想学习、视觉再认、图片回忆)、日常生活能力量表(ADL),比较2组患者上述量表评分和MMSE、MoCA量表各亚项评分的差异.结果 与对照者比较,MCI患者MMSE、MoCA总分和RVR、WAIS-RC、WMS-R分测验,MoCA量表各亚项(地点定向力除外),MMSE量表中计算与注意、延迟回忆两亚项评分较低,差异均有统计学意义(P<0.05).结论 MCI患者不仅记忆受损,其计算与注意力、命名、视空间结构能力、执行功能也可受损,尤以延迟回忆、计算与注意力受损明显.MoCA涵盖了重要的认知领域,能较全面评估MCI患者的认知功能,值的临床推广应用.     

血清胆红素和尿酸浓度与轻度认知障碍的相关性研究

目的探讨轻度认知功能障碍(MCI)患者血清胆红素和尿酸水平与认知功能的关系。方法检测71例MCI患者(MCI组)及80名认知正常者(对照组)患者的血尿酸、总胆红素(TB)、直接胆红素(DBIL)、间接胆红素(IBIL)水平。采用MMSE和蒙特利尔认知评估量表(MoCA)对入组者行神经心理学评定。结果与对照组比较,MCI组年龄及吸烟史比率显著升高(均P0.05),受教育年限、MMSE评分、MoCA评分、MoCA子评分中的视空间与执行能力、注意力、抽象思维、延迟回忆及TB、IBIL、尿酸浓度显著降低(P0.05～0.01)。TB与MMSE、MoCA评分呈正相关(r=0.287,P=0.030;r=0.347,P=0.024),与MoCA子项目中的视空间与执行功能、抽象思维、延迟回忆呈正相关(r=0.327,P=0.040;r=0.310,P=0.028;r=0.315,P=0.038)。尿酸与MMSE、MoCA评分呈正相关(r=0.293,P=0.030;r=0.337,P=0.013),与MoCA子项目中的视空间与执行功能、注意力、延迟回忆、抽象思维呈正相关(r=0.300,P=0.021;r=0.318,P=0.013;r=0.302,P=0.020;r=0.296,P=0.025)。多因素Logistic回归分析显示,高龄、低教育程度和吸烟是MCI的独立危险因素(P0.05～0.01),TB及尿酸水平是MCI的保护性因素(均P0.05)。结论高龄、低教育程度和吸烟可促进MCI发生,TB及尿酸水平可防止MCI。     

2型糖尿病患者轻度认知功能障碍的临床分析

目的探讨2型糖尿病患者轻度认知功能障碍的特点。方法将122例2型糖尿病患者分为伴2型糖尿病轻度认知功能障碍组(45例)、不伴2型糖尿病轻度认知功能障碍组(41例)和对照组(36例),使用蒙特利尔认知评估量表(montreal cognitive assessme,MoCA)对患者的命名、注意、视空间/执行功能、持续注意、语言、计算、抽象、定向力、延迟回忆进行评分评估。结果与对照组比较,伴2型糖尿病轻度认知功能障碍组在命名、注意、视空间/执行功能、持续注意、语言、计算、抽象、定向力、延迟回忆等评分比较差异具有统计学意义(P0.01)。与不伴2型糖尿病MCI组比较,伴2型糖尿病MCI组在总分、视空间/执行功能、注意、持续注意、延迟回忆等评分2组间差异有统计学意义(P0.05)。结论伴2型糖尿病的MCI患者在命名、注意、视空间/执行功能、持续注意、语言、计算、抽象、定向力、延迟回忆等方面有不同程度的损害;其总体认知功能损害较不伴2型糖尿病者严重,尤其在视空间/执行能力、注意、持续注意及记忆方面。     

帕金森病轻度认知功能障碍的临床特点

目的 探讨帕金森病患者轻度认知功能障碍(PD-MCI)的临床特点。方法 纳入85例非痴呆的帕金森病(PD)患者,并进行临床资料的采集及相关量表评估。结果 PD-MCI组55例(64.7%),PD-认知正常组30例(35.3%)。PD-MCI组的年龄及发病时年龄显著高于PD-认知正常组(P<0.05),PD-MCI组MoCA评分中的视空间与执行功能、注意、语言、抽象、延迟回忆得分显著低于PD-认知正常组(P<0.01)。PD-MCI组的MoCA评分与UPDRS Ⅲ评分及发病年龄呈负相关,与受教育水平呈正相关。结论 与认知功能正常的PD患者比较,PD-MCI患者在视空间与执行功能、注意、语言、抽象、延迟回忆等方面均有损害,且认知损害程度与发病年龄、运动症状严重程度及受教育水平有关。     

脑白质病变患者认知功能的前瞻性研究

目的 探讨不同部位和严重程度脑白质病变（white matter lesions,WMLs）患者的认知功能损害特点。 方法 前瞻性纳入179例WMLs病例和97例磁共振成像（magnetic resonance imaging,MRI）正常对照组, 并收集人口学资料,对WMLs的严重程度进行Fazekas视觉等级评分,依据WMLs病变部位分为皮质下脑 白质病变（subcortical white matter lesions,SWML）组、脑室旁脑白质病变（periventricular lesions,PVL）组 和混合组,采用蒙特利尔认知评估量表（Montreal Cognitive Assessment Scale,MoCA）分析不同部位和 严重程度WMLs的认知功能差异。根据MoCA将WMLs组分为WMLs认知损害亚组（116例）及WMLs认知正 常亚组（63例）,分析探讨WMLs患者认知损害的危险因素。 结果 与正常组比,WMLs组在MoCA总分（P ﹤0.001）、视空间与执行能力（P ﹤0.001）、命名（P =0.019）、 语言（P =0.005）、抽象理解（P =0.003）、延迟记忆（P ﹤0.001）方面显著性减低。Fazekas分级越高, MoCA总分及各项评分显著减低（P均﹤0.05）。PVL组、SWML组和混合组与对照组相比,在MoCA总分（P 均﹤0.001）、视空间与执行能力（P 均﹤0.001）、语言（P =0.006,0.022,0.008）、抽象理解（P =0.003, 0.011,0.016）及延迟记忆（P均﹤0.001）上差异有统计学意义。WMLs亚组分析显示高教育程度是WMLs发 生认知损害的保护因素。 结论 高教育程度是WMLs患者认知损害的保护因素。WMLs患者在视空间与执行功能、延迟回忆方面 存在明显的认知损害。WMLs病变程度越严重,认知功能下降越显著。皮质下WMLs、脑室旁WMLs及混 合组均在视空间与执行能力、语言、抽象理解、延迟记忆方面损害严重。     

帕金森病患者的轻度认知功能障碍

目的评估帕金森病(Parkinson’s disease,PD)患者的认知功能状态,分析帕金森病合并轻度认知功能障碍(Parkinson’s Disease with Mild Cognitive Impairment,PD-MCI)的特点。方法纳入PD患者64例,采用神经心理测试组评估其注意、视空间、执行和记忆等认知域的功能。结果本组PD患者中,认知功能正常24例(37.5%),PD-MCI 30例(46.9%),帕金森病痴呆10例(15.6%)。在PD-MCI患者中,单个认知领域轻度损害(60.0%)较多个认知域型轻度认知损害(40.0%)更常见,累及较多的认知域依次为记忆(20例,66.7%),执行(13例,43.3%),视空间(12例,36.7%)。早期PD患者PD-MCI发生率为36.4%,痴呆发生率为3.0%;中晚期PD患者PD-MCI发生率为58.1%,痴呆发生率达29.0%,两组差异有显著性(χ2=18.222,P<0.001)。PD患者的病情程度与认知功能状态呈负相关(Spearman相关系数=-0.553,P<0.001)。结论轻度认知功能障碍(mild cogni-tive impairment,MCI)在PD患者中常见,即使在疾病早期,其发生率也较高,其中单个认知领域轻度损害较多个认知域型轻度认知损害更常见。PD患者的病情越严重,认知功能状态越差。     

动脉硬化性脑小血管病与阿尔茨海默病认知功能损害特征的比较

目的 比较动脉硬化性脑小血管病（arteriosclerotic cerebral small vessel disease，aCSVD）与阿尔茨海 默病（Alzheimer’s disease，AD）患者认知功能损害特征。 方法 回顾性收集2017年9月-2019年5月中山大学附属第三医院神经内科临床诊断为aCSVD及AD患 者的一般资料、认知功能评估量表（MMSE及MoCA），比较两组患者的血管危险因素及认知功能损害 特征的差异。 结果 aCSVD组共纳入106例，AD组88例。aCSVD组患者年龄较低、BMI较高、高血压患者比例较 高，差异均具有统计学意义。MMSE量表各子项评分比较，aCSVD组的注意力与计算力、执行评分低于 AD组，AD组的定向力、延迟回忆、复述、理解及书写评分低于aCSVD组；MoCA量表各子项评分比较， aCSVD组的视空间与执行功能、数字递减评分低于AD组，AD组的命名、数字重复、语言能力、抽象能 力、延迟回忆及定向力评分低于aCSVD组，差异均具有统计学意义。 结论 aCSVD认知障碍发病年龄低于同等认知程度的AD组。aCSVD认知损害维度以注意力与计算力、 视空间与执行功能损害为主，而AD以定向力、延迟回忆、语言能力损害为主。     

晚发型抑郁障碍与轻度认知功能损害患者的认知功能差异研究

目的 探讨晚发型抑郁障碍患者与轻度认知功能损害患者的认知功能损害的差异.方法 研究对象为2012年7月～2013年8月上海市精神卫生中心老年科住院与门诊就诊符合DSM—Ⅳ诊断标准且起病年龄≥60岁的抑郁障碍患者,共26例为晚发型抑郁障碍组（LOD组）,另选择26例轻度认知功能损害的患者（MCI组）与26例正常老年人（NC组）.认知功能评估采用简明精神状态量表（MMSE）、蒙特利尔量表（MoCA）.结果 MMSE总分、MMSE分测验中计算力与注意力及MoCA总分、MoCA分测验中连线、注意、持续注意、计算、复述、延迟回忆在LOD组与MCI组差比较异无统计学意义（P＞0.05）,两组与NC组比较差异有统计学意义（P＜0.05）.三组在MMSE分测验的时间定向、延迟回忆、三步指令、书写书面指令及MoCA分测验的复制图、画钟、命名比较,MCI组均值最低,与NC组比较差异有统计学意义（P＜0.05）,与LOD组比较差异无统计学意义（P＞0.05）.结论 LOD组认知功能在注意力、延迟回忆、连线测验方面与MCI组损害程度相当.MCI组认知功能受损范围较LOD组广泛.     

Diagnostic Difficulties and Treatment Implications

Summary: Differentiation between types of epileptic seizures has been aided in recent years by the introduction of intensive neurodiagnostic techniques and the development of increasingly detailed classification systems. Paradoxically, these developments have not simplified the task of matching the appropriate antiepileptic drug to a particular seizure type. It is reasonable to assume that anticonvulsant drugs will have different effects on different types of seizures, but faulty, circular reasoning can enter the picture if one also assumes that responses of seizures to different drugs signify different seizure types. There are several examples of differential diagnoses that can fall prey to this problem, including the diagnosis between partial seizures with secondary generalization and generalized tonic-clonic seizures, and the diagnosis between complex partial seizures and absence seizures with automatisms, among others. Considerations of etiology in future classification systems can further complicate the problem: should one then choose an anticonvulsant drug on the basis of individual seizure type or on the basis of the type of epilepsy? Ramifications of this issue extend even to the drug approval process. Official sanction is not given for use of a drug for a seizure type not included in the original efficacy studies, even if later scientific evidence shows that seizure type to be related to a type that is included. New trials must be undertaken. These problems arise from how we choose to classify seizures.     

Cognitive Dysfunction Associated with Antiepileptic Drug Therapy

Summary: Epilepsy is frequently associated with cognitive dysfunction. However, the reasons for this correlation are unclear. Possible influential factors include patient age; duration, frequency, etiology, and type of seizures; hereditary factors; psychosocial issues; and antiepileptic drug (AED) therapy. Whereas many of these factors are beyond the physician's control, AED therapy is one element that can be addressed in treatment decisions by recognizing the potential cognitive effects of particular AEDs. For example, phenobarbital impairs memory and concentration; phenytoin affects attention, problem solving ability, and performance of visuomotor tasks. In contrast, carbamazepine may affect concentration, while valproate would appear to have minimal effects on cognition. Moreover, cognitive effects of AEDs are amplified with coadministration of multiple anticonvulsants (polytherapy). A review of studies on the cognitive effects of monotherapy with AEDs, as opposed to those of polytherapy, provides evidence that drug-related cognitive dysfunction can be reversed if patients are switched to a simpler therapeutic regimen. Future research should be directed toward developing reliable measures for assessing and monitoring cognition, and understanding the particular cognitive side effects of each AED. Physicians also need to revise their opinions about which side effects are "tolerable" for epileptic patients.     

Epilepsy and anomalies of neuronal migration: MRI and clinical aspects

Neuronal migration disorders are the result of disturbed brain development. In such disorders, neurons are abnormally located. In diagnosing these conditions, magnetic resonance imaging is superior to any other imaging technique. This enables us to improve our knowledge of the clinical correlates of neuronal migration. With reference to migrational disorder, a retrospective study of all 303 patients with epileptic seizures referred for magnetic resonance imaging during a 3-year period was performed, 13 patients (aged 12-41, mean age 27) were identified. They represent 4.3% of the entire study group. Of the patients with known epilepsy, 6.7% and of the mentally retarded, 13.7% had migrational disorders. Four patients had schizencephaly as the dominant finding, one was classified as hemimegalencephaly, 2 had isolated heterotopias, and 6 had localized pachy- and/or poly-microgyria. The clinical pictures are complex. Ectopias of grey matter are recognised foci of epilepsy, but from an epileptological and a clinical viewpoint little attention has been given to these disorders. The present study shows that malmigration is not rare in epilepsy patients, especially not in the mentally retarded.     

Carbamazepine Efficacy in Adults With Partial and Generalized Tonic-Clonic Seizures

Summary: Carbamazepine and phenytoin are drugs of choice in initial monotherapy for adult partial and secondarily generalized tonic-clonic seizures. These designations reflect the results of the Veterans Administration Epilepsy Cooperative Study Group of 1985. An earlier comparative study of carbamazepine and phenytoin by Ramsay and associates found both drugs equally effective in controlling new-onset seizures. Among the advantages of carbamazepine is that it causes relatively few cognitive and dysmorphic side effects. Its disadvantages are its unavailability in parenteral formulation and its metabolic autoinduction. The latter must be compensated for by planned dosage increases to maintain therapeutic plasma steady-state levels during the first 2 or 3 months of treatment. Carbamazepine is judged a drug of choice in the treatment of these secondarily generalized tonic-clonic seizures, and the drug of choice in children, adolescents, and women susceptible to the dysmorphic side effects associated with other anticonvulsant agents.     

Etiologic and Preventive Aspects of Epilepsy in the Child–Bridging the Gap Between Laboratory and Clinic

Summary: Four broad categories of basic phenomena are pertinent to developing ways to prevent epilepsy. These include mechanisms of epileptogenesis, ictal initiation and temporary entrainment by the seizure discharge of normally functioning brain, seizure propagation, and control mechanisms that function both to restrain the cascade of epileptic events culminating in a seizure and to arrest the epileptic event and restore the interictal state. In newborns and children, hypoxia-ischemia is a major factor leading to epileptogenesis, and several schemes are proposed to classify, quantify, and prevent hypoxic-ischemic encephalopathy. Control mechanisms must be better understood in order to develop prophylactic recommendations for epilepsy, and an experimental model of "kindling antagonism" may increase our understanding of these. Programs of prevention of seizures in children will evolve only if basic researchers and clinicians work productively together to develop an adequate understanding of factors important in epileptogenesis and antiepileptogenic control mechanisms.     

Predisposing and Causative Factors in Childhood Epilepsy

Summary: We review information from large studies of defined populations, examining the role of known factors and especially of prenatal and perinatal factors in contributing to nonfebrile seizure disorders of early childhood. We depend especially, but not exclusively, on the recently completed analyses from the Collaborative Perinatal Project of the National Institute of Neurological and Communicative Disorders and Stroke, the NCPP. About 4% of children in the NCPP who had at least one non-febrile nonsymptomatic seizure by the age of 7 years had a previous seizure during acute neurologic illness, such as meningitis or during the acute illness after trauma. Many such seizures should potentially be preventable. Of children with seizures, 10% had had a neonatal seizure and 13% had had a febrile seizure. Among the hundreds of prenatal and perinatal factors explored as predictors of childhood seizure disorders, the principal predictors identified were congenital malformations of the fetus, cerebral and noncerebral; family history of certain neurologic disorders; and neonatal seizures. In agreement with the British National Child Development Study, labor and delivery factors in the NCPP appeared to contribute very little to childhood seizure disorders. Maldevelopment, rather than damage at birth to an initially intact nervous system, appeared to be the more common mechanism. Most seizure disorders of early childhood remained unexplained by the large set of prenatal and perinatal characteristics examined.     

Classification of methods in transcranial Electrical Stimulation (tES) and evolving strategy from historical approaches to contemporary innovations

Transcranial Electrical Stimulation (tES) encompasses all methods of non-invasive current application to the brain used in research and clinical practice. We present the first comprehensive and technical review, explaining the evolution of tES in both terminology and dosage over the past 100 years of research to present day. Current transcranial Pulsed Current Stimulation (tPCS) approaches such as Cranial Electrotherapy Stimulation (CES) descended from Electrosleep (ES) through Cranial Electro-stimulation Therapy (CET), Transcerebral Electrotherapy (TCET), and NeuroElectric Therapy (NET) while others like Transcutaneous Cranial Electrical Stimulation (TCES) descended from Electroanesthesia (EA) through Limoge, and Interferential Stimulation. Prior to a contemporary resurgence in interest, variations of transcranial Direct Current Stimulation were explored intermittently, including Polarizing current, Galvanic Vestibular Stimulation (GVS), and Transcranial Micropolarization. The development of these approaches alongside Electroconvulsive Therapy (ECT) and pharmacological developments are considered. Both the roots and unique features of contemporary approaches such as transcranial Alternating Current Stimulation (tACS) and transcranial Random Noise Stimulation (tRNS) are discussed. Trends and incremental developments in electrode montage and waveform spanning decades are presented leading to the present day. Commercial devices, seminal conferences, and regulatory decisions are noted. We conclude with six rules on how increasing medical and technological sophistication may now be leveraged for broader success and adoption of tES.     

Treatment Considerations in Anticonvulsant Monotherapy

Summary: The long-standing practice of polypharmacy in treating epilepsy is giving way to use of monotherapy. Monotherapy can improve seizure control as well as reduce the risk of serious idiosyncratic reactions, dose-related side effects, and complex drug interactions. Monotherapy also offers improved compliance and cost-effectiveness. The basis of monotherapy is accurate diagnosis and assessment of the patient's seizure type(s), followed by selection of a single appropriate anticonvulsant drug. Many patients currently treated with multiple anticonvulsants can be successfully converted to monotherapy with a carefully monitored program in which troublesome and redundant drugs are gradually withdrawn from the therapeutic regimen.     

Anticonvulsant Drugs and Cognitive Function: A Review of the Literature

Summary: Alterations of cognitive function are separate from disturbances of behavior seen in association with epilepsy. The nature of the cognitive disability may to a certain extent depend on the seizure type. Partial seizures, mainly derived from a temporal lobe focus, impair memory tasks, while generalized seizures seem to have more effect on attentional abilities. A number of studies, reviewed in this paper, suggest that anticonvulsant drugs further impair cognitive function. Maximal impairments are seen in patients receiving polytherapy: rationalization of polytherapy improves cognitive abilities. Studies in children and adults have allowed differentiation of the effects of various commonly used antiepileptic agents. Maximal cognitive deficits are seen with. phenytoin, while phenobarbital and sodium valproate induce moderate disturbances, and carbamazepine seems relatively free from such toxicity. Further research is needed on the interrelationship between types of seizure disorders, types of anticonvulsant medications, and cognitive function.     

Dextromethorphan: Cellular Effects Reducing Neuronal Hyperactivity

Summary: Dextromethorphan is a dextrorotary morphinan without affinity for opioid receptors, commonly used as an antitussive medication. During the past 5 years, interest in the compound and its demethylated derivative, dextrorphan, has been revived because additional neuroprotective and an-tiepileptic properties were found in in vitro studies, animal experiments, and a few clinical cases. Both morphinans are able to inhibit N -methyl-D-aspartate (NMDA) receptor channels and voltage-operated calcium and sodium channels with different potencies. The inhibition of the NMDA receptor is believed to be the predominant mechanism of action responsible for the anticonvulsant and neuroprotective properties of the compounds.