葛根素治疗腔隙性脑梗死的疗效观察

葛根素具有抗血栓、改善微循环、提高缺血区血流量作用[1].本院采用葛根素治疗腔隙性脑梗死,现报告如下.1对象与方法1.1对象系2010年本科收住的360例腔隙性脑梗死患者,均符合全国第四届脑血管病学术会议修订的诊断标准,并经头颅影像学检查证实.随机分为两组,(1)葛根素组:182例,男96例,女86例;年龄42～ 71岁,平均(63.4±13.1)岁;病程13～ 37 h,平均(22.2±9.5)h;美国国立卫生研究院卒中量表(NIHSS)评分8～ 17分,平均(13.2±1.4)分.(2)对照组:178例,男93例,女85例;年龄41 ～72岁,平均(63.3±13.1)岁;病程12 ～36 h,平均(22.1±9.4)h;NIHSS评分7～17分,平均(13.2±1.4)分.两组患者在年龄、性别、病程及病情差异无统计学意义.     

血浆同型半胱氨酸与腔隙性脑梗死及认知功能关系

目的:探讨血浆同型半胱氨酸(Hcy)与腔隙性脑梗死的关系以及对认知功能的影响。方法:选取112例腔隙性脑梗死患者及50名健康对照者,检测血浆Hcy水平以及简易智能精神状态检查表(MMSE)评分。结果:①Hcy水平腔隙性脑梗死组明显高于对照组(P<0.05);②Logistic回归证实Hcy水平升高是腔隙性脑梗死的独立危险因素,OR为1.212;③Hcy水平与MMSE分值呈负相关(r=-0.552,P<0.001);④多元线性回归分析得出腔隙性脑梗死患者MMSE分数=45.771-7.314×logHcy-0.171×年龄。结论:血浆Hcy水平升高是腔隙性脑梗死的独立危险因素,对认知功能有独立的影响。     

不同形态腔隙性脑梗死与预后的关系

目的分析穿支动脉病变引起的腔隙性脑梗死形态与其预后的关系。方法收集2011年6月至2013年9月广西脑卒中中心通过磁共振弥散加权成像(diffusion weighted imaging,DWI)确诊的急性腔隙性脑梗死患者,并根据DWI特征,把急性腔隙性脑梗死的梗死形态分为椭圆形和串珠形。对两种形态脑梗死患者的人口形态特征、危险因素、入院和出院时的NIH卒中评分以及出院3个月后Ranking评分进行评估,同时分析其卒中机制。结果共纳入189例患者,其中串珠状脑梗死69例(36.5%),而椭圆形脑梗死120例(63.5%)。两组患者的基线无差别。然而串珠形梗死组最大梗死直径较椭圆形组大(13.8±2.3 mm vs.10.6±3.2 mm,P=0.006)。早期神经功能恶化同样在串珠形脑梗死组较椭圆形组更常见(24.6%vs.5.0%,P=0.009)。早期神经功能恢复在串珠形脑梗死患者更差(30.5%vs.10.8%,P=0.018)。多元Logistic回归分析显示:串珠形脑梗死病灶与早期神经功能恶化有关(OR=7.55,95%CI:1.73~33.25,P=0.010),而与早期神经功能恢复不良有关(OR=5.75,95%CI:1.53~28.70,P=0.030)。结论在穿支病变引起的腔隙性脑梗死中,串珠状脑梗死与早期神经功能恶化及早期神经功能恢复不良显著相关。     

脑小血管病影像总负荷与急性脑梗死静脉溶栓远期预后的相关性研究

目的研究CSVD影像学总负荷与急性脑梗死静脉溶栓远期预后的相关性。方法回顾性连续收集我院2018年1月-2020年1月收治的发病4.5 h之内经重组组织型纤溶酶原激活剂(rt-PA)静脉溶栓的急性脑梗死患者124例,收集患者的一般基线资料,发病48 h之内行头颅MRI检查,根据Staals等的评分标准,评估患者CSVD影像学总负荷评分为0~4分,通过电话随访评估患者90 d mRS评分,根据mRS评分将患者分为预后良好组(mRS:0~2分)和预后不良组(mRS:3~5分),比较2组患者的一般资料及影像学CSVD评分有无差异。结果124例脑梗死静脉溶栓患者远期预后基线资料的单因素分析发现预后良好患者82例(66%),预后不良患者42例(34%),静脉溶栓早期有出血转化患者10例,其中HI-1型8例,PH-1型2例,2组出血转化差异无统计学意义(P>0.05),无死亡患者。2组患者基线资料比较显示溶栓前NIHSS评分、溶栓前舒张压水平、高密度脂蛋白胆固醇水平、既往房颤病史、既往心衰病史、既往脑梗死病史、TOSTA分型、CSVD影像总负荷两组间差异有统计学意义(P<0.05)。其余资料比较两组间差异无统计学意义(P>0.05)。多因素Logistic回归分析结果显示溶栓前NIHSS评分(OR=1.241,95%CI 1.125~1.370,P<0.001)、高CSVD总评分(OR=2.393,95%CI 1.493~3.873,P<0.001)是影响脑梗死静脉溶栓预后的独立危险因素;CSVD不同影像表现中WMH中重度(OR=2.560,95%CI 1.158~5.662,P<0.020)和腔隙性脑梗死(OR=5.030,95%CI 1.579~16.044,P<0.006)是预后的独立危险因素。结论急性脑梗死静脉溶栓患者CSVD影像总负荷评分较高者与90 d不良预后相关,影像学表现为腔隙性脑梗死及中重度的WMH是不良预后的独立危险因素。     

缺血性脑卒中亚型及其危险因素与脑白质变性的关系

目的探讨缺血性脑卒中亚型及其危险因素与脑白质变性(LA)的关系。方法对213例伴LA的缺血性脑卒中患者的LA程度进行分级(LA1、LA2、LA3),分析其与缺血性脑卒中亚型(短暂脑缺血发作、腔隙性脑梗死、动脉血栓形成和心源性脑梗死)及其危险因素(年龄、性别、高血压、糖尿病及冠心病等)的关系。结果213例伴LA的缺血性脑卒中患者中,LA2和LA3患者的年龄明显高于LA1患者(均P<0.05);腔隙性脑梗死患者LA3的发生率明显高于其他缺血性脑卒中亚型(均P<0.05);与LA程度明显相关的因素为年龄(OR 0.69,95%CI:0.49~0.97)和腔隙性脑梗死(OR 0.01,95%CI:0.00~0.33)(均P<0.05)。结论与LA相关的危险因素是高龄和腔隙性脑梗死;可能的机制为穿支动脉硬化和血压调节障碍影响脑白质血流供应,引起白质局部坏死、腔隙形成或弥漫性LA。     

急性腔隙性脑梗死患者血清C-反应蛋白和白介素-8水平的变化及临床意义

目的 探讨急性腔隙性脑梗死患者血清高敏C-反应蛋白(hs-CRP)、白介素-8水平(IL-8) 的变化及在发病机制中的作用.方法 分别检测36例腔隙性脑梗死、36例脑梗死和36例健康对照者血清hs-CRP和IL-8含量.结果 腔梗组和脑梗组hs-CRP含量分别为(10.42±0.68)、(18.45±1.28)mg/L,均显著高于对照组的(1.28±0.47)mg/L(P＜0.01),CI组hs-CRP含量亦显著高于健康对照组(P＜0.01);腔梗组和脑梗组IL-8含量分别为(29.65±18.24)、(36.57±19.01)ng/ml,显著高于对照组的(25.98±16.87)ng/ml(P＜0.01),在脑梗患者中,大面积脑梗死(≥9ml)hs-CRP为(21.36±1.48)mg/L,显著高于小面积脑梗死组(<9ml)的(15.30±0.97)mg/L(P＜0.01),2组IL-8含量分别为(38.1±19.87)、(33.45±18.67)ng/ml,差异亦有统计学意义(P＜0.01).结论 炎症过程参与了脑小血管病变;hs-CRP和IL-8水平与脑缺血程度以及脑的小血管病变范围密切相关.hs-CRP 及IL-8是预测脑梗死患者病情严重程度的重要生化指标.     

腔隙性脑梗死合并脑微出血临床及影像学特征研究

目的探讨腔隙性脑梗死患者合并脑微出血(cerebral microbleeds,CMBs)的临床及其影像学特征。方法采用前瞻性研究方法,连续收集2013年8月~2015年9月在本院神经内科住院的腔隙性脑梗死患者120例,根据有无CMBs将患者分为有CMBs组(39例)和无CMBs组(81例),比较2组间基本临床资料、生化指标及影像学特点是否存在差异,并采用多因素逐步Logistic回归模型分析CMBs发生的独立危险因素。结果 120例腔隙性脑梗死患者中合并CMBs39例(32.5%),其中2组年龄(t=6.373,P0.001)、高血压病(χ~2=5.385,P=0.02)、高尿酸(χ~2=4.474,P=0.04)、腔隙性脑梗死数目(t=8.773,P0.001)以及脑白质疏松程度评分(t=7.964,P0.001)比较差异具有统计学意义。Logistic回归分析显示,年龄、高血压病、腔隙性脑梗死数目以及脑白质疏松程度评分是腔隙性脑梗死患者发生CMBs的独立危险因素。结论腔隙性脑梗死患者CMBs发生与年龄、高血压病、腔隙性脑梗死数目以及脑白质疏松程度有关。     

脑小血管病总负荷对大动脉粥样硬化型脑梗死急性期病情进展的影响

目的探讨脑小血管病(cerebral small vessel disease,CSVD)总负荷与大动脉粥样硬化(large artery atherosclerosis,LAA)型脑梗死急性期病情进展的关系。方法143例急性LAA型脑梗死患者,依据MRI检查及CSVD总负荷评分量表计算患者的CSVD总负荷评分(总分0~4分)。根据急性期病情有无进展,将患者分为两组:非进展性脑梗死组(non-progressive cerebral infarction,NPCI)和进展性脑梗死组(progressive cerebral infarction,PCI),比较两组间基线资料及CSVD各分项及总负荷评分间的差异,并应用Logistic回归法分析CSVD总负荷评分等指标与LAA型脑梗死急性期进展的关系。结果PCI组与NPCI组间CSVD总负荷评分程度有显著性差异(P<0.05)。PCI组吸烟史、糖尿病史、基线舒张压、空腹血糖、血管源性腔隙、中重度脑白质病变(WMH)、脑微出血(CMBs)及CSVD总负荷评分均高于NPCI组(P<0.05),低密度脂蛋白胆固醇(LDL-C)低于NPCI组(P<0.05);Logistic回归分析显示:空腹血糖、中重度WMH以及CSVD总负荷评分是LAA型脑梗死急性期病情进展的独立危险因素(P<0.05)。结论LAA型脑梗死患者CSVD总负荷严重程度与急性期病情进展密切相关。     

颈动脉粥样硬化斑块性质与血清C-反应蛋白的关系

目的 探讨颈动脉粥样硬化斑块性质与血清C-反应蛋白(CRP)水平的关系.方法 对经多层螺旋CT血管成像(MSCTA)检测发现有颈动脉粥样硬化斑块的28例脑血栓形成、24例腔隙性脑梗死、19例颈内动脉系统TIA患者进行CRP测定,分析斑块的性质与血清CRP水平的关系.结果 (1)脑血栓形成组和TIA组以混合性斑块和软斑块为主,腔隙性脑梗死组以硬斑块为主;3组间斑块类型分布差异有统计学意义(均P<0.05);(2)血清CRP水平:脑血栓形成组为(4.022±1.531)mg/L,腔隙性脑梗死组为(3.781±1.876)mg/L,TIA组为(3.920±2.155)mg/L,3组间CRP水平差异无统计学意义(均P>0.05);(3)不同斑块组的CRP水平:软斑块组为( 4.546±2.720) mg/L,混合性斑块组为(3.951±1.863)mg/L,显著高于硬斑块组[(2.762±1.323)mg/L](均P<0.05).结论 血清CRP水平对判断颈动脉粥样硬化斑块的稳定性具有一定临床意义.     

急性腔隙性脑梗死患者血清C反应蛋白和白介素-8水平的变化及临床意义

目的 探讨急性腔隙性脑梗死患者血清高敏C反应蛋白(hs-CRP)、白介素-8水平(IL-8) 的变化及其在发病机制中的作用.方法 分别检测36例腔隙性脑梗死和36例脑梗死患者及36例健康对照者血清hs-CRP和IL-8含量.结果 腔梗组和脑梗组hs-CRP含量分别为(10.42±0.68)mg/L和(18.45±1.28)mg/L,均显著高于对照组的(1.28±0.47)mg/L(P<0.01),CI组hs-CRP含量亦显著高于健康对照组(P<0.01);腔梗组和脑梗组IL-8含量分别为(29.65±18.24)ng/ml和(36.57±19.01)ng/ml,显著高于对照组的(25.98±16.87)ng/ml(P<0.01).在脑梗患死者中,大面积脑梗死组(≥9ml,n=16)hs-CRP为(21.36±1.48)mg/L,显著高于小面积脑梗死组(<9ml,n=20)的(15.30±0.97)mg/l(P<0.01),2组IL-8含量分别为(38.1±19.87)ng/ml和(33.45±18.67)ng/mL,差异亦有统计学意义(P<0.01).结论 炎症过程参与了脑小血管病变;hs-CRP和IL-8水平与脑缺血程度以及脑的小血管病变范围密切相关.hs-CRP 及IL-8是预测脑梗死患者病情严重程度的重要生化指标.     

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.     

Hepatic Considerations in the Use of Antiepileptic Drugs

Summary: Virtually all of the major antiepileptic drugs (AEDs) can cause hepatotoxicity, although fatal hepatic reactions are rare. The mechanisms, incidences, and risk profiles for such reactions differ from drug to drug. With carbamazepine and phenytoin, hepatotoxicity may be due to drug hypersensitivity. Although the profiles of patients at risk have not been well-defined for these two antiepileptic drugs, it would appear from reports in the literature that older adolescents and adults are at higher risk than children of developing serious or fatal hepatotoxicity. Once hepatotoxicity develops, mortality rates are 10–38% with phenytoin and 25% for carbamazepine. The risk profile for valproate fatal hepatotoxicity has been more clearly defined. Those at primary risk of fatal hepatic dysfunction are children under the age of 2 years who are receiving multiple anticonvulsants and also have significant medical problems in addition to severe epilepsy. The risk is considerably lower for patients over the age of 2 years on valproate monotherapy. In contrast to the risk profile with other AEDs, adults receiving valproate as monotherapy have the lowest risk of hepatotoxicity. Fatal hepatic dysfunction coincident with valproate may be the result of aberrant drug metabolism. Concomitant use of AEDs that induce microsomal P450 enzymes (e.g., phenytoin and phenobarbital) may enhance the production of a toxic metabolite, and hence the greater risk of hepatotoxicity with polypharmacy.     

Vascular Malformations and Epilepsy: Clinical Considerations and Basic Mechanisms

Summary: Vascular malformations (VMs) are associated with epilepsy. The natural history of the various VMs, clinical presentation, and tendency to provoke epilepsy determine treatment strategies. Investigations have probed the mechanisms of epileptogenesis associated with these lesions. Electrophysiologic changes are associated with epileptogenic cortex adjacent to VMs. Putative pathophysiologic mechanisms of epileptogenesis include neuronal cell loss, glial proliferation and abnormal glial physiology, altered neurotransmitter levels, free radical formation, and aberrant second messenger physiology.     

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.     

Carbamazepine Efficacy and Utilization in Children

Summary: Carbamazepine is effective for preventing partial and generalized tonic-clonic seizures in children. Although absence epilepsies are more common in children than adults, an estimated 80% of children with epilepsy have seizure types or epilepsies that are potentially responsive to carbamazepine. The differential diagnosis of ictal staring is an especially important issue in children because absence and atypical absence seizures are more prevalent in children than adults. Age-related pharmacokinetic differences and drug interactions are major considerations in children. On average, children have higher clearance rates of carbamazepine, shorter half-lives, and higher ratios of carbamazepine-10, 11-epoxide to carbamazepine than adults. In addition, children with severe epilepsy are more likely to require multiple-drug therapy, which can lead to complex drug interactions. When carbamazepine is administered along with valproate, drug protein binding interactions can cause intermittent side effects.     

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.     

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.