640层螺旋CT脑灌注成像与CT血管成像在超早期脑梗死中的应用

目的探讨东芝Aquilion ONE 640层CT脑灌注成像(CTP)与CT血管成像(CTA)在超早期脑梗死患者中的应用价值。方法我院2014-06—2015-12收治的28例超早期脑梗死患者,均在发病后6h内实施CT平扫、CTP与CTA检查,分析平扫及灌注CT表现,计算CTP的达峰时间(TTP)、脑血流量(CBF)、脑血容量(CBV)各参数值,并与对侧及半暗带周边相应区灌注参数相对比;重建颈段和脑内动脉CTA图像,采用图像后处理技术显示病变血管情况,对动脉狭窄程度进行分级评价。所有患者3~7d内行多层螺旋CT复查,评估CTP与CTA在超早期脑梗死诊断中的临床价值。结果 28例患者经头颅CT平扫发现,11例有可疑脑缺血区,其余17例未见明显异常。行CT脑血管灌注成像发现,患者感兴趣区内rCBF、rCBV、rTTP(病变侧与对照侧灌注参数的相对比值)明显改变,脑梗死区较边缘区TTP更高,CBF、CBV更低,差异均有统计学意义(P0.01);半暗带区CBF、TTP与对侧比较差异有统计学意义(P0.01),而CBV对比差异无统计学意义(P0.05)。CTA检查发现,10例患者大脑中动脉闭塞,7例大脑中动脉狭窄,11例一侧颈内动脉狭窄或闭塞。结论 CTP早期发现脑梗死患者脑组织中的缺血半暗带,CTA检查可准确判断狭窄或闭塞血管,在脑梗死患者的早期诊断和指导溶栓治疗中有重要临床价值。     

急性脑梗死动脉内药物溶栓和机械支架再通比较

目的观察急性脑梗死患者脑血管特点,比较动脉内尿激酶溶栓、机械再通和支架成形的安全及有效性。方法对发病1．5—8h的11例急性腩梗死患者,行全脑血管数字减影（DSA）造影,给予动脉内治疗;进行血管再通评价,美国国立卫生院神经功能缺损评分（National Institutes of Health Stroke Scale,NIHSS）和1个月改良Rankin量表评分。结果术前NIHSS为6～21。责任血管闭塞6例（54．5％）;重度狭窄3例（27．3％）;未见异常2例（18．2％）。2例闭塞粗管行闭塞局部尿激酶溶栓,未再通,术后1例出血死亡,1例大面积脑梗死,改良Rankin量表评分为5;3例血管闭塞行机械再通后支架成形;1例同侧责任血管闭塞伴对侧颈内动脉重度狭窄和3例同侧责任血管重度狭窄行狭窄处支架成形,术后血管均再通,无出血;2例DSA检查未见异常病例仅药物治疗。后3组1个月改良Rankin量表评分为0～1。结论急性脑梗死时对于闭塞施管机械再通较尿激酶溶栓血管再通可靠,对于重度狭窄血管可行支架治疗。     

急性缺血性脑血管病76例多模式CT影像学分析

目的探讨76例急性缺血性脑血管病(AICVD)的多模式CT影像学特点。方法采用320排多层螺旋CT对76例AICVD(发病时间24h)患者急诊进行CT平扫(NCCT)+CT灌注成像(CTP)+CT血管成像(CTA)一站式扫描检查,分析灌注区脑血流量(CBF)、脑血容量(CBV)、平均通过时间(MTT)、达峰时间(TTP)等灌注参数变化及CT血管成像(CTA),并于入院后3d内行头颅MRI,评估其脑灌注特点及血管影像。结果在获取的76例CTP数据中,通过感兴趣区识别划分筛查,有59例患者有明确的异常CTP,有17例患者未发现明确感兴趣区。59例异常CTP中包括急性脑梗死47例,短暂性脑缺血发作(TIA)12例。急性脑梗死患者异常CTP特点:发病在4.5h以内的4例患者CTP表现为患侧CBF均较健侧下降,CBV正常或者轻度增高,MTT、TTP延长;发病时间在4.5~6h内的4例:其中2例CTP表现为CBF降低,CBV正常,MTT、TTP延长,2例表现为CBF降低,CBV轻度降低,MTT、TTP延长;发病时间在6~24h内的39例:其中30例梗死区与CTP异常脑灌注区部位一致,均表现CBF明显降低,CBV明显降低,MTT、TTP延长;12例TIA患者CTP均发现与临床症状相对应的灌注异常:MTT、TTP延长,CBF正常或减低,CBV升高。CTA发现责任动脉重度狭窄5例,血管闭塞10例,7例可见血流缓慢,排空延迟及侧支血管形成。结论多模式CT能够对AICVD提供血流灌注参数的变化及血管情况、供血区的血流动力学变化,对临床诊治具有一定参考价值,主要用于评估大脑半球卒中,多模式CT有临床价值。     

糖尿病与非糖尿病性急性脑梗死患者脑血管狭窄程度的比较

目的比较糖尿病（DM）与非糖尿病（NDM）性急性脑梗死患者脑血管狭窄程度。方法DM性脑梗死患者（DM脑梗死组）51例及糖耐量正常的脑梗死患者作为对照组（NDM脑梗死组）64例，均行全脑数字减影血管造影（DSA）检查，比较颅内外血管狭窄或闭塞情况。结果两组均以颅内动脉狭窄为常见，主要为大脑中动脉M1、M2段，颈内动脉颅外段等，其中DM脑梗死组血管异常率84．31％，NDM脑梗死组异常率70．31％；在DM脑梗死组中血管病变以多支狭窄（52．94％）为主，合并溃疡或斑块39．21％，11．63％存在侧支循环；而NDM脑梗死组中多支狭窄为18．75％，合并溃疡或斑块为17．19％，侧支循环形成为31．11％，两组间比较差异有统计学意义（均P＜0．05）；但两组所涉及的血管病变部位差异无统计学意义（P〉0．05）。结论DM性脑梗死的血管病变范围广泛．多支血管病蛮发牛率高、程摩萤．     

症状性和无症状性颈内动脉狭窄的大脑中动脉微栓子信号监测

目的观察症状性和无症状性颈内动脉狭窄的患者大脑中动脉微栓子信号（microembolicsig-nals,MES）阳性率及MES计数的变化,研究微栓子与临床症状和颈内动脉狭窄程度的关系。方法选取症状性颈内动脉狭窄患者26例,无症状性颈内动脉狭窄患者20例及正常对照组30例;症状性颈内动脉狭窄组又分为短暂性脑缺血发作（transient ischemic attack,TIA）组（12例）和脑梗死组（14例）;症状性和无症状性颈内动脉狭窄的患者均行DSA或CTA检查,并对颈内动脉狭窄程度进行分级;所有颈内动脉狭窄的患者均对颈内动脉狭窄同侧的大脑中动脉进行MES监测,正常对照组则对双侧大脑中动脉进行MES监测。结果有症状和无症状颈内动脉狭窄组的MES阳性率高于正常对照组（P〈0．01）;有症状颈内动脉狭窄组MES阳性率较无症状组高（P〈0．05）;TIA组和脑梗死组比较,MEs阳性率无显著性差异（P〉0．05）;症状性和无症状性颈内动脉狭窄患者,轻、中、重度狭窄三组的MES阳性率比较均有显著性差异（P〈0．05）;MES阳性患者MES计数与颈内动脉狭窄程度呈正相关（r=0．9155,P〈0．01）。结论MES多见在颈内动脉狭窄患者,特别是症状性颈内动脉狭窄的患者,是缺血性脑血管疾病发生的高危因素。     

腔隙性脑梗死102例患者的脑血流动力学分析

目的 依据神经影像学资料分析腔隙性脑梗死患者脑和血管病变及其发病机制。方法 对102例腔隙性脑梗死患者进行头颅MRI、CT血管造影（CTA）、CT灌注成像（CTP）检查。结果 单发腔隙性脑梗死3例，多发腔隙性脑梗死99例。CTA显示颈内动脉（ICA）重度狭窄或闭塞32例，轻-中度狭窄19例。中动脉（MCA）重度狭窄或闭塞11例，轻-中度狭窄5例。ICA或MCA粥样硬化23例，正常血管12例。CTP显示ICA-MCA供血区内血流灌注异常56例。结论 腔隙性脑梗死可能由大动脉狭窄或闭塞所造成的远端小动脉血流灌注减低和微栓子所致。     

后循环动脉狭窄支架植入前后血流动力学变化的初步研究

目的探讨症状性椎-基底动脉狭窄内支架成形术前后脑血流动力学变化。方法回顾性分析38例症状性椎一基底动脉狭窄病人的临床资料,其中中度狭窄32例,重度狭窄6例。病人均行血管内支架成形术,手术前后行经颅彩色多普勒（TCD）及脑CT灌注成像（CTP）检查,测量狭窄处血流速度峰值及平均脑血容量（CBV）、平均脑血流量（CBF）、平均通过时间（MTT）。结果支架成彤术后,动脉狭窄处血流速度峰值由术前的（226±27）cm／s降至（135±18）cm／s,差异有统计学意义（P〈O．01）。直接供血区术后MTT较术前明显降低（P〈0．01）,CBF较术前明显增高（P〈O,05）,CBV较术前无明显改变（P〉0．05）。结论TCD联合CTP可评估症状性椎一基底动脉狭窄内支架成形术后脑灌注改善情况。     

急性脑梗死患者脑动脉狭窄或闭塞后梗死灶体积的影响因素

目的：探讨急性脑梗死患者脑动脉狭窄或者闭塞后梗死灶体积的影响因素。方法选取2015年1～12月收入我院神经内科的急性脑梗死患者80例为研究对象,采用 mRS 评分判断患者的临床转归情况,采用 ROC 曲线预测患者临床转归梗死灶体积的最佳切点,采用 Logistic 多因素回归模型分析影响梗死灶体积的因素。结果梗死灶体积≤29．23 ml 时,其临床转归的效果较好,且灵敏度及特异度较高,ROC 曲线下面积为0．997。梗死灶体积≤29．23 ml 组和梗死灶体积＞29．23 ml 组患者,在年龄、NIHSS 评分、白细胞数、血清白蛋白、hs － CRP 、GHbA1c 水平及脑白质疏松程度方面比较,差异有统计学意义（P ＜0．05）。 Logistic 多因素分析显示,血清白蛋白是脑动脉狭窄或者闭塞后梗死灶体积＞29．23 ml 的保护因素（P ＜0．05）,GHbA1c 和脑白质疏松程度是危险因素（P ＜0．05）。结论血清白蛋白、GHbA1c 水平和脑白质疏松程度是急性脑梗死患者脑动脉狭窄或者闭塞后梗死灶体积的影响因素。     

颈内动脉急性闭塞致大面积脑梗死侧支循环建立及影响因素

目的评估颈内动脉急性闭塞致大面积脑梗死侧枝循环建立情况及影响因素。方法纳入29例经诊断为颈内动脉急性闭塞致大面积脑梗死的患者,所有患者均行颈动脉超声、经颅多普勒超声(TCD)、头颅CT、头颅磁共振血管造影(MRA)、心电图检查,同时收集患者基本信息。结果一级侧枝循环建立与糖尿病显著相关(P 0. 05),与房颤、高血压、吸烟、NIHSS评分无关(P 0. 05)。二级侧枝循环建立与房颤、高血压、糖尿病、吸烟、NIHSS评分均无关(P 0. 05)。心源性脑栓塞导致的急性大面积脑梗死与脑疝显著相关(P 0. 05)。TCD评估一级侧枝循环的建立与MRA具有高度一致性(Kappa值=0. 656,P 0. 05)。结论糖尿病可促进颈内动脉急性闭塞导致的大面积脑梗死一级侧枝开放。心源性脑栓塞导致的大面积脑梗死易发生脑疝。TCD可以较好评估颈内动脉急性闭塞导致的大面积脑梗死的一级侧枝循环建立。     

头颅CT灌注成像在球囊闭塞试验中的辅助作用

目的探讨头颅CT灌注成像（CTP）在球囊闭塞试验（BOT）中的辅助判断作用。方法 20例经DSA确诊的颈内动脉巨大动脉瘤患者,临床判断为BOT阴性的同时行头颅CTP,通过比较双侧半球的脑血流量（CBF）、脑血容量（CBV）及达峰时间（TTP）对脑血流动力学进行评估。结果 20例患者均在BOT过程中完成CTP且无任何脑缺血症状,17例（85.0%）灌注对称,判断为耐受性良好,16例行永久性颈内动脉球囊闭塞术（其中4例联合动脉瘤部分栓塞术）,1例行颈内动脉慢性阻断术;3例（15.0%）灌注不对称,主要为阻断侧TTP延长,CBV正常或轻度升高,而CBF基本正常,即存在早期的脑血流动力学损害,认为其无法耐受颈内动脉的永久闭塞,其中2例行颅内外动脉搭桥联合动脉瘤孤立术,1例行支架辅助的动脉瘤致密栓塞术,载瘤动脉保留完整。所有患者随访15～32个月,均无远期缺血并发症。结论 CTP能检出BOT阴性者潜在的脑血流动力学损害,可以更客观地评估其对颈内动脉永久闭塞的耐受力,是BOT的重要补充。     

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.     

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 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.     

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.