DTI评价轻度认知障碍及轻中度阿尔茨海默病脑白质微细结构损害的研究

目的应用磁共振弥散张量成像(DTI)技术研究轻度认知障碍(MCI)及轻中度阿尔茨海默病(AD)患者脑白质微细结构的改变。方法对MCI患者、轻中度AD患者各12例及健康老年人12名(对照组)行常规MRI及DTI检查,测量其胼胝体压部、额叶、顶叶、颞叶、枕叶、内囊前肢及内囊后肢白质区部分各向异性分数(FA)和平均弥散率(MD)。将3组的FA、MD值进行比较,并与MMSE评分、单词回忆及单词再认评分进行相关性分析。结果 (1)MCI患者顶叶白质FA值为0.489±0.079,与对照组(0.558±0.079)相比下降(P0.05)。(2)AD患者额叶、顶叶及颞叶FA值分别为0.405±0.072、0.454±0.069和0.363±0.056,与对照组(分别为0.499±0.081、0.558±0.079和0.440±0.061)比较差异均有统计学意义(P0.05)。AD患者胼胝体压部、额叶及顶叶MD值分别为0.978±0.082、0.920±0.054和0.81 7±0.045,均高于对照组(分别为0.801±0.093、0.820±0.084、0.712±0.096)(P0.05)。AD、MCI两组内囊前、后肢及枕叶FA及MD值分别与健康对照组比较均无统计学差异(P0.05)。(3)3组顶叶、颞叶FA值与MMSE、单词回忆及单词再认评分均有相关性(分别r=0.869、-0.621、-0.759,均P0.01;r=0.446、-0.486、-0.361,均P0.05),胼胝体压部FA值与单词再认评分有相关性(r=-0.343,P0.05);3组胼胝体压部及顶叶MD值与MMSE、单词回忆及单词再认评分均有相关性(分别r=-0.612、0.547、0.586,均P0.01;r=-0.576、0.499、0.519,均P0.01),内囊前肢MD值与MMSE评分相关(r=-0.340,P0.05)。结论 MCI及轻中度AD患者存在脑白质选择性微细结构损害,且该损害出现在与高级皮层功能相关的脑区,而与初级功能相关的区域未见明显受损。     

磁共振扩散张量成像在缺血缺氧脑病患儿中的临床应用

目的探讨磁共振扩散张量成像(DTI)在缺血缺氧脑病患儿中的应用价值。方法前瞻性纳入2016-12—2018-12于河南中医药大学第一附属医院行MRI头颅平扫及DTI检查的年龄2岁患儿40例,所有患儿在围生期均有缺氧缺血脑病史,根据最终随访结果分为脑瘫组及非脑瘫组各20例。测量双侧大脑脚、内囊前肢、内囊膝部、内囊后肢、半卵圆中心、皮质脊髓束、下纵束、丘脑后辐射、额叶白质、顶叶白质、胼胝体膝部、胼胝体体部及胼胝体压部的FA值。结果 2组间双侧大脑脚、内囊后肢、半卵圆中心、皮质脊髓束、下纵束、丘脑后辐射、顶叶白质、胼胝体膝部、胼胝体体部、胼胝体压部FA值差异均有统计学意义(P0.05),而双侧内囊前肢、内囊膝部、额叶白质FA值差异无统计学意义(P0.05)。结论 DTI可以定量评估缺血缺氧脑病患儿的损伤程度,有助于早期评估病情及预测预后。     

弥散张量成像对阿尔茨海默病脑白质改变的评价

目的分析阿尔茨海默病(Alzheimer's disease,AD)脑白质结构改变及与认知功能的关系。方法对37例AD组和32例对照组行简易精神状态量表(mini-mental State examinationn,MMSE)评估和DTI扫描。采用基于全脑体素分析法对两组全脑白质各向异性(fractional anisotropy,FA)图进行比较,采用t检验分析FA值差异,并评估AD组MMSE评分与FA值相关性。结果 AD患者出现FA值下降区域广泛分布在右侧额叶、颞叶、枕叶、丘脑及双侧扣带回、胼胝体、楔前叶、顶叶下回、顶下小叶、缘上回及海马旁回(其中P0.001,未经校正的P值);当使用经FWE校正的P0.05后,AD患者右侧扣带回、左侧胼胝体、颞叶下回及双侧顶叶下回、额叶下回、楔前叶区域FA值较对照组显著下降。AD患者FA值下降与MMSE量表评分呈正相关,(P0.001,未经校正)。结论 AD患者存在特定脑区白质结构改变,并与认知功能损害程度呈正相关。     

皮质下缺血性血管性痴呆患者脑白质损害的磁共振弥散张量成像研究

目的:应用磁共振弥散张量成像技术(DTI)观察皮质下缺血性血管性痴呆(SIVD)患者脑白质损害程度,探讨DTI对SIVD白质损害的评估及与阿尔茨海默病(AD)鉴别诊断价值。方法:研究对象分为3组,分别是健康老年人(NC)、皮质下缺血性血管性痴呆(SIVD)患者、AD患者,每组各20例。行常规MR I和DTI扫描后,测定相同感兴趣区(RO I)的各向异性分数(FA)值和表观扩散系数(ADC)值进行比较。结果:SIVD组下额枕束、胼胝体膝部、胼胝体压部、上纵束等部位FA值下降,ADC值升高,与NC、AD组比较差异有统计学意义(P<0.05)。与NC组比较,AD组前额叶、颞叶、海马、下额枕束、胼胝体膝部和扣带束等部位FA值降低,颞叶、海马等部位ADC值升高,两组差异具有显著性(P<0.05);结论:DTI可以用来评估痴呆患者白质损害的程度,SIVD患者以下额枕束、胼胝体膝部、胼胝体压部、上纵束等部位受累为主,可作为与AD鉴别的客观指标。     

轻度认知功能障碍与脑白质弥散张量成像的相关性研究

目的通过磁共振弥散张量成像研究不同区域脑白质损害与轻度认知功能(MCI)的关系。方法纳入2015年7月至2016年2月我院的住院患者56例为研究对象,其中MCI组34例,认知功能正常组22例。所有研究对象进行一般情况检查,完成神经心理学量表检测。通过头颅磁共振弥散张量成像(DTI)检查对不同脑区白质纤维进行部分各向异性(FA)值测量。结果 MCI组患者与认知功能正常组相比,右侧额叶FA值(0.335±0.068)、左侧颞叶白质FA值(0.391±0.032)及胼胝体膝部FA值(0.658±0.053)降低,差异具有统计学意义(P0.05)。将上述FA值和MMSE、Mo CA量表中各认知域进行典型相关分析,结果显示右侧额叶白质FA值与注意与计算力呈正相关,左侧颞叶白质和胼胝体膝部FA值与记忆力呈正相关(P0.05)。结论 MCI患者注意与计算力的障碍可能与右侧额叶白质损害有关,而左侧颞叶白质及胼胝体膝部白质的损害可能导致早期的记忆障碍。DTI可能成为超早期识别与诊断MCI的新方法。     

皮质下缺血性血管性认知损害扩散张量成像研究

目的通过扩散张量成像(DTI)探讨皮质下缺血性血管性认知损害患者白质微结构变化及其与认知功能之间的相关性。方法采集49例皮质下缺血性脑血管病患者[轻度血管性痴呆(VaD)10例、非痴呆型血管性认知损害(VCIND)20例、认知功能正常19例]DTI数据并观察皮质下白质微结构改变,分析VaD组患者DTI参数与认知功能间的相关性。结果与对照组相比,VaD组内侧前额叶、前扣带回、胼胝体干、双侧顶叶、右侧颞叶、双侧眶额叶,以及VCIND组右侧额下回、右侧海马、双侧楔前叶FA值减低(均P=0.000);与VCIND组比较,VaD组内侧前额叶、前扣带回、胼胝体、双侧顶叶、右侧颞叶FA值减低(P=0.000)。与对照组相比,VaD组内侧前额叶、胼胝体、双侧顶叶、双侧颞叶、前扣带回,以及VCIND组双侧楔前叶、右侧海马MD值升高(均P=0.000);与VCIND组相比,VaD组右侧内侧前额叶、前扣带回、胼胝体干、双侧顶叶、双侧颞叶MD值升高(均P=0.000)。VaD组内侧前额叶FA值与数字连线测验A时呈显著负相关(r=-0.782,P=0.007),双侧额下回MD值与数字连线试验A时程呈显著正相关(r=0.877,P=0.001)。结论 DTI对皮质下缺血性认知损害患者白质微结构改变更敏感,能够反映患者认知功能早期异常改变;内侧前额叶白质微结构的改变是影响患者执行能力的重要因素。     

额叶癫(癎)执行功能损害及磁共振弥散张量成像研究

目的用磁共振弥散张量成像技术研究额叶癫患者执行功能损害的相关脑区及病理改变,探讨其可能的发生机制。方法对32例成人额叶癫患者和75例正常健康对照者进行神经心理检查,并对18例常规影像无病灶的额叶癫患者和20例正常健康对照者进行弥散张量成像扫描及统计分析。结果额叶癫患者组语义流畅性明显差于对照组,数字广度测验得分和90min正确填写数字符号个数明显低于对照组。与对照组比较,额叶癫患者右侧额叶MD值明显高于对照组;右侧外囊、尾状核和双侧丘脑的FA值明显低于对照组,差异具有显著性意义。相关分析显示双侧内囊前肢、左侧外囊、左枕叶皮质下白质FA值与语义流畅性呈正相关。左侧内囊膝部、内囊后肢和丘脑MD值与MMSE呈负相关;双侧内囊前肢、左侧外囊、额叶、枕叶相应白质内FA值与MMSE呈正相关。结论DTI显示额叶癫患者右侧额叶MD值明显增高、右侧外囊、尾状核和双侧丘脑的FA值明显减低,提示额叶癫患者在上述区域可能存在细微病理改变,执行功能可能超出前额叶的范围。     

癫(癎)患者磁共振弥散张量成像及其与智能损害的关系

目的 采用磁共振弥散张量成像技术研究癫(癎)患者智能损害的相关脑区及病理改变,探讨其可能的发生机制.方法 对44例癫(癎)患者和20名健康人进行韦氏成人量表和磁共振弥散张量成像检查.结果 癫(癎)组患者的全量表智商(FIQ,98.19±17.76)、语言智商(VIQ,100.52±17.63)、操作智商(PIQ,95.10±16.72)均显著低于对照组(VIQ:109.77±13.54、PIQ:108.11±12.17、FIQ:109.81±10.57).癫(癎)智能缺损患者胼胝体膝部平均扩散率(MD值)高于癫(癎)智能正常组,双侧内囊前肢、左侧内囊膝部、左侧外囊、双侧枕叶白质和双侧壳核的各向异性(FA)值低于癫(癎)智能正常组,差异有统计学意义(P＜0.05).相关分析发现,右枕叶FA值与FIQ呈正相关;右侧额叶MD值与VIQ呈负相关;右侧枕叶FA值与VIQ呈正相关;两侧枕叶FA值均与PIQ正相关.结论 本组癫(癎)患者在FIQ、VIQ、PIQ均存在损害.癫(癎)患者伴有智能缺损的胼胝体膝部平均扩散率增加,双侧内囊前肢、左侧内囊膝部、左侧外囊、双侧枕叶白质和双侧壳核各向异性减低;枕叶的各向异性减低与FIQ减低有关,额叶平均扩散率增加与VIQ减低有关,皮质下白质在认知中可能起较重要的作用.     

额叶癫痫执行功能损害及磁共振弥散张量成像研究

目的用磁共振弥散张量成像技术研究额叶癫痫患者执行功能损害的相关脑区及病理改变，探讨其可能的发生机制。方法对32例成人额叶癫痫患者和75例正常健康对照者进行神经心理检查，并对18例常规影像无病灶的额叶癫痫患者和20例正常健康对照者进行弥散张量成像扫描及统计分析。结果额叶癫痫患者组语义流畅性明显差于对照组，数字广度测验得分和90min正确填写数字符号个数明显低于对照组。与对照组比较，额叶癫痫患者右侧额叶MD值明显高于对照组；右侧外囊、尾状核和双侧丘脑的FA值明显低于对照组，差异具有显著性意义。相关分析显示双侧内囊前肢、左侧外囊、左枕叶皮质下白质FA值与语义流畅性呈正相关。左侧内囊膝部、内囊后肢和丘脑MD值与MMSE呈负相关；双侧内囊前肢、左侧外囊、额叶、枕叶相应白质内FA值与MMSE呈正相关。结论DTI显示额叶癫疴患者右侧额叶MD值明显增高、右侧外囊、尾状核和双侧丘脑的FA值明显减低，提示额叶癫痫患者在上述区域可能存在细微病理改变，执行功能可能超出前额叶的范围。     

Duchenne型肌营养不良症扩散张量成像研究

目的通过扩散张量成像(DTI)观察Duchenne型肌营养不良症患儿脑结构和功能改变。方法共14例Duchenne型肌营养不良症患儿均行DTI检查,以双侧顶叶白质、额叶白质、胼胝体膝部和压部、尾状核头、扣带前回、扣带中回、扣带后回、豆状核、内囊前肢和后肢、丘脑、枕叶白质、颞叶白质、海马、小脑上脚和小脑中脚等脑区为兴趣区,测定各兴趣区部分各向异性(FA)值。结果与正常对照者相比,Duchenne型肌营养不良症患儿仅胼胝体压部FA值降低(t=-2.187,P=0.045),其余脑区FA值组间差异均无统计学意义(P0.05)。结论 Duchenne型肌营养不良症患儿胼胝体压部存在微细结构改变,然而,其与Duchenne型肌营养不良症患儿认知功能改变之间的相关性尚待进一步研究。     

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.     

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.     

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.     

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.     

Effects of NMD A- and AMPA-Receptor Antagonists on Different Forms of Epileptiform Activity in Rat Temporal Cortex Slices

Summary: Lowering extracellular magnesium induces different patterns of epileptiform activity in rat hippocampus and entorhinal cortex. Short recurrent epileptiform discharges in the hippocampus are stable over time, whereas seizurelike events (SLEs) in the entorhinal cortex, the subiculum, and the neighboring neocortex develop into late recurrent discharges which are not blocked by clinically employed antiepileptic drugs. We tested the sensitivity of the different epileptiform discharge patterns to. /V-methyl-D-aspartate (NMDA)- and non-NMDA-receptor antagonists. As NMDA-receptor antagonist we used dextrorphan, ket-amine, and 2-aminophosphonovalerate (2APV); as α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA)-receptor antagonist we employed the quinoxaline derivative glutamate 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). The findings show that the different patterns of epileptiform activity, including the late recurrent discharges, are sensitive to all NMDA-receptor antagonists. However, when dextrorphan was employed to suppress seizure-like events, later recurrent discharges did not develop during the remaining time course of the experiment. CNQX reversibly suppressed recurrent discharges in the hippocampus and SLEs in the entorhinal cortex. However, late recurrent discharges become insensitive to CNQX, even at a high concentration of 60 μM m. This finding suggests a prominent role for NMDA receptors in the generation of late recurrent discharges.