缺血性卒中患者颅内外动脉狭窄与高血压、糖尿病的研究

目的 探讨缺血性卒中患者的颅内外动脉狭窄特点及程度与高血压病、糖尿病的病史及控制水平的 关系。 方法 回顾性分析住院治疗的存在颅内外动脉狭窄且并发高血压或糖尿病的大动脉粥样硬化性急 性缺血性卒中患者资料。将高血压患者分为高年限组（病史>5年）和低年限组（病史≤5年）,血压 控制良好组和不良组;将糖尿病患者也分为高年限组（病史>5年）和低年限组（病史≤5年）,血糖 控制良好组和不良组。比较不同组间颅内外动脉狭窄分布情况、血管狭窄程度。 结果 共入组216例急性缺血性卒中患者,其中57例颅外动脉狭窄,105例颅内动脉狭窄,54例颅内 外动脉均狭窄。轻度狭窄发生73例,中度狭窄发生101例,重度狭窄及闭塞发生42例。高血压病患者 共140例,高年限组动脉狭窄最常见于颅内动脉（54.5%）,低年限组血管狭窄的部位多见于颅外动脉 （51.3%）,差异有统计学意义（P＜0.001）。两组间动脉狭窄程度差异也有统计学意义。糖尿病患者共 76例,高年限组发生动脉狭窄最常见于颅内动脉（72.2%）,低年限组血管狭窄的部位多见于颅外动脉 （65%）,差异有统计学意义,两组间动脉狭窄程度差异也有统计学意义。高血压控制不良组发生重度 狭窄或闭塞的概率高于血压控制良好组（20.7% vs 8.6%）;血糖控制情况不良组发生重度狭窄或闭 塞的概率高于血糖控制良好组（40.9% vs 6.3%）。 结论 随着高血压病年限的增长,急性缺血性卒中患者颅内动脉狭窄的发生率增高,其中以中度狭 窄程度多见;血压控制不良的患者发生重度狭窄或闭塞的比率高。随着糖尿病年限的增长,颅内动 脉狭窄的发生率增高,其中以中度狭窄程度多见,血糖控制不良者发生重度狭窄或闭塞的比例高。     

脑卒中后糖尿病和糖调节异常的临床研究

目的调查脑卒中患者中糖尿病和糖调节异常的发病情况，探讨口服葡萄糖耐量试验（OGTT）的临床意义。方法对2004年1月-2006年6月收治入院的547例脑卒中患者进行空腹血糖、糖化血红蛋白（GHbAlc）等检测，登记患者的临床资料，对既往未诊断糖尿病而空腹血糖在5．6～6．9mmol／L的患者在适当时候进行OGTT，糖代谢分类采用2003年美国糖尿病学会建议标准。结果547例脑卒中患者住院前糖尿病的诊断率为13.9％，住院后检查发现糖尿病的患病率34．4％，糖调节异常26．5％；脑梗死、脑出血、蛛网膜下腔出血糖尿病的伴发率分别为45．1％、20．5％、13．2％，糖调节异常的伴发率分别30．2％、23．2％、16．2％；227例空腹血糖在5．6～6．9mmol／L的患者中，OGTT检查后发现，19．8％患者可诊断为糖尿病，42.3％提示糖耐量异常。结论脑卒中患者合并高比例的糖尿病和糖调节异常；缺血性卒中发病率高于出血性卒中：空腹血糖在5．6～6．9mmol／L的患者中，OGTT可以发现大量的糖尿病和糖耐量异常患者。     

50例脑动脉重度狭窄（闭塞）分布及相关危险因素分析

目的研究脑动脉重度狭窄（闭塞）的血管分布及其相关危险因素,为缺血性脑卒中的发病机制、临床诊断、治疗以及预防提供重要依据。方法通过对50例DSA和（或）CTA诊断为脑动脉重度狭窄（或闭塞）的缺血性脑卒中患者计算其重度狭窄或闭塞动脉数目及其分布,同时测血压、血糖（GLU）、尿酸（UA）、甘油三酯（TC）、总胆固醇（TG）、高密度脂蛋白（HDL-C）、低密度脂蛋白（LDL-C）、极低密度脂蛋白（VLDL-C）、外周血白细胞数（WBC）、血小板数（PLT）、血小板分布宽度（PDW）、平均血小板体积（MPV）、大血小板比率（P—LCR）及纤维蛋白原（FIB）,与无脑动脉狭窄纽比较以上相关因素的差异。结果颅内动脉重度狭窄率（84．6％）明显高于颅外动脉（15．4％）,比较脑动脉存在重度狭窄与无狭窄的两组缺血性脑卒中患者,其舒张压、UA、TC、LDL-C、VLDL-C、WBC、PLT、PDW、MPV、P—LCR差异均无统计学意义（P〉0．05）,而收缩压、FIB、GLU、TG、HDL-C、年龄因素差异有统计学意义（P〈0．05或P〈0．01）,Logistic回归发现高血压、糖尿病与缺血性脑卒中脑动脉重度狭窄呈明显相关性（P〈0．05）。结论缺血性脑卒中患者颅内动脉重度狭窄发生率高于颅外动脉,HDL-C水平与脑动脉狭窄呈负相关,高血压、糖尿病与脑动脉重度狭窄有关,而高血压是脑动脉重度狭窄的独立危险因素。     

缺血性卒中患者动脉狭窄分布及变化趋势

目的 探讨缺血性卒中狭窄的分布及变化趋势。方法 缺血性卒中患者230例行全脑血管造影,根据年龄分为＜60岁组（121例）和≥60岁组（109例）,比较不同组患者脑供血动脉狭窄程度的差异。结果 ≥60岁组颈动脉颅外段和后循环颅外段狭窄的比率较＜60岁组高（P＜0.01）;＜60岁组颅内动脉闭塞较≥60岁组多见（P＜0.01）,＜60岁组颅内动脉闭塞较同组颅外动脉闭塞多见（P＜0.01）。结论 不同年龄缺血性卒中患者狭窄血管的空间分布及变化趋势不同。     

特发性脑动脉夹层28例致缺血性卒中机制分析

目的 通过回顾分析特发性脑动脉夹层（cerebral artery dissection,CAD）患者影像学和血管学资料研究其缺血性卒中机制,为治疗策略提供依据。方法 选取28例特发性CAD所致急性缺血性卒中患者,根据缺血性卒中病灶形态和分布来确定CAD致缺血性卒中机制;根据夹层病变的位置分为颅内组和颅外组,对两组患者夹层致缺血性卒中机制进行比较。结果 共28例患者纳入研究,男19例,女9例。颅外组17例,其中颈内动脉夹层15例,椎动脉V1段夹层2例。颅内组11例,其中大脑中动脉M1段夹层3例,基底动脉夹层2例,椎动脉V4段夹层6例。颅内组高血压和糖尿病患者分别为7例（63.6%）和5例（45.5%）,颅外组均为1例（5.9%）,颅内组高血压和糖尿病患病比例多于颅外组（P =0.002,0.022）。颅外组和颅内组单纯栓塞性缺血性卒中分别有12例（70.6%）和2例（18.2%）,两组比较差异有统计学意义（P =0.018）。颅内组由夹层病变闭塞局部穿支动脉所致缺血性卒中7例（63.6%）,由夹层闭塞穿支合并血流动力学机制所致1例（9.1%）,单纯血流动力学机制所致1例（9.1%）。结论 颅外CAD致缺血性卒中机制与颅内CAD有所不同,前者主要导致栓塞性缺血性卒中,而后者致缺血性卒中机制主要为夹层病变闭塞局部穿支动脉。     

支架技术在急性缺血性卒中合并颅内外动脉狭窄中的应用

目的探讨支架技术在急性缺血性卒中合并颅内外动脉狭窄中应用的可行性、安全性及有效性。方法回顾性纳入2014年4月至2016年10月在山东大学附属济南市中心医院神经外科就诊的29例急性缺血性卒中合并颅内外动脉狭窄的患者。经数字减影血管造影（DSA）证实责任动脉闭塞,患者取栓后仍有重度狭窄,遂行球囊扩张、支架置入血管成形术。记录患者治疗前、后7d美国国立卫生研究院卒中量表（NIHSS）评分、30d卒中或短暂性脑缺血性发作的复发率及90d改良Rankin量表评分（mRS）。临床随访分别在术后30d和90d进行。结果29例患者的技术成功率为100％,支架治疗后平均残留狭窄率为（10．4±8．1）％。所有患者均得到随访,30d内再次卒中1例。NIHSS评分：治疗前为（19．5±3．5）分,治疗后7d为（5．8±2．1）分,治疗前后的差异有统计学意义（P〈0．05）。90d患者的病死率为0％,其中28例（97％）90dmRS评分≤2分,预后良好。结论急性缺血性卒中合并颅内动脉狭窄患者应用支架技术的并发症发生率较低且安全、有效;但残余狭窄以及合并基础性疾病、医嘱依从性差被认为是卒中再发的危险因素。     

缺血性卒中患者颅内动脉狭窄的相关危险因素分析

目的 探讨颅内动脉狭窄的狭窄程度、相关危险因素与缺血性脑卒中的关系,为缺血性卒中的防治提供重要依据.方法 90例缺血性卒中患者根据全DSA检查结果分为非狭窄组(狭窄<30%)与颅内动脉狭窄组(狭窄≥30%或闭塞),分析颅内动脉狭窄程度与年龄、性别、高血压、糖尿病、高脂血症、冠心病、家族史、总胆固醇(CHO)、三酰甘油(TG)、高密度脂蛋白胆同醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白 A1(ApoA1)、载脂蛋白B(ApoB)、血清脂蛋白(Lpa)等相关危险因素的关系.结果 (1)本组患者颅内动脉狭窄发生率为67.78%,发生率最高为大脑巾动脉,其次颈内动脉颅内段和椎基底动脉颅内段,发生率最低为大脑后动脉.(2)有高血压、糖尿病的缺血性卒中患者容易发生颅内动脉狭窄,其同归系数、OR值、P值分别为1.659、5.256、0.002,1.657、5.241、0.046.(3)颅内动脉狭窄组HDL-C含量[(0.99±0.30)mmol/L]比非狭窄组[(1.30±0.50)mmol/L]明显降低,差异有统计学意义(t=3.603,P=0.001).(4)年龄、性别、吸烟、既往卒中史、脑血管病家族史、TC、TG、LDL-C、ApoA1、ApoB、Lpa在两组间比较差异无统计学意义(P>0.05).结论 缺血性卒中患者颅内血管狭窄的主要危险因素有高血压、糖尿病,保护因素有HDL-C.     

急性缺血性卒中患者颅内动脉粥样硬化性狭窄与不同血糖水平代谢综合征的相关性分析

目的 探讨急性缺血性卒中患者颅内动脉粥样硬化性狭窄与不同血糖水平代谢综合征的相关性。 方法 选取2013年6月-2016年6月入住本院神经内科的急性缺血性卒中患者352例为研究对象,根 据颅内血管狭窄情况分为狭窄组227例和非狭窄组125例;选取同期非颅内动脉粥样硬化性狭窄体检 者310例为对照组。研究对象中合并代谢综合征的患者分为3个亚组：糖耐量正常组、伴糖尿病组、伴 高血糖组（包括空腹血糖受损、糖耐量降低）。同时测定代谢综合征患者血脂水平,分析不同血糖 水平代谢综合征与颅内动脉粥样硬化性狭窄的相关性。 结果 352例急性缺血性卒中患者共确诊代谢综合征195例（55.39%）,其中狭窄组和非狭窄组代谢 综合征的发生率均明显高于对照组,比较差异有显著性（P <0.05）;狭窄组代谢综合征的发生率明显 高于非狭窄组,比较差异有显著性（P <0.05）。狭窄组中伴糖尿病的代谢综合征患者比例明显高于非 狭窄组和对照组,比较差异有显著性（P <0.05）;狭窄组中伴高血糖和糖耐量正常的代谢综合征患 者比例与非狭窄组比较,差异均无显著性（P＞0.05）。Logistic回归分析显示：代谢综合征与颅内动脉 粥样硬化性狭窄存在明显相关性;代谢综合征伴糖尿病、伴低高密度脂蛋白（high density lipoprotein, HDL）、高甘油三酯（triglyceride,TG）与颅内动脉粥样硬化性狭窄发生风险呈明显正相关。 结论 在急性缺血性卒中患者中,代谢综合征尤其是糖尿病、高TG血症及低HDL血症和颅内动脉粥 样硬化性狭窄密切相关。     

缺血性卒中患者颅内外血管狭窄率研究

目的:研究缺血性卒中患者颅内外血管狭窄或闭塞的发生率,并对其相关病因进行分析。方法:对经CT/MRI/DWI诊断的缺血性卒中患者的人口构成情况进行登记,了解其相关危险因素。并经TCD和/或MRA了解其颅内外血管狭窄或闭塞的情况。结果:579例缺血性卒中患者中,颅内外血管狭窄的发生率为70.98%(411/579例);411例大动脉狭窄或闭塞患者中,以大脑中动脉狭窄或闭塞最常见(64.48%),其次为颈内动脉(50.36%)。大动脉狭窄或闭塞的主要原因为动脉粥样硬化,引起动脉粥样硬化的危险因素的发病率依次为:高血压病(77.24%),吸烟(63.68%)。通过Logistic回归分析发现,糖尿病、高血压、吸烟是血管狭窄的主要相关危险因素(P值均<0.05)。结论:国内缺血性卒中患者颅内外血管狭窄或闭塞的发生率高,其主要病因为动脉粥样硬化,糖尿病是大动脉狭窄或闭塞的最主要危险因素。     

颅内外动脉粥样硬化相关因素的差异

目的 探讨颅内外动脉粥样硬化的相关因素是否存在差异。 方法 在中国颅内动脉粥样硬化研究的数据库中,将患者分为4组：无显著颅内外动脉狭窄或闭塞组、 单纯颅内动脉病变组、单纯颅外动脉病变组及颅内合并颅外动脉病变组。以无显著颅内外动脉狭窄 或闭塞组作为参考,应用多元Logistic回归分析,评估颅内外动脉病变的相关因素。 结果 共入组2864例缺血性脑血管病患者,其中无显著颅内外动脉狭窄或闭塞组1388例（48.5%）、 单纯颅内动脉病变组1074例（37.5%）、单纯颅外动脉病变组141例（4.9%）、颅内合并颅外动脉 病变组261例（9.1%）。多因素分析显示,单纯颅内动脉病变的独立相关因素包括：白质病变[比值比 （odds ratio,OR）1.359,95%（confidence interval,CI）1.109～1.666,P =0.0031] 、白细胞计数（OR 1.045, 95%CI 1.007～1.084,P =0.0210）、空腹血糖（OR 1.054,95%CI 1.009～1.101,P =0.0182）、高密度脂 蛋白（OR 0.644,95%CI 0.480～0.864,P =0.0034）;单纯颅外动脉病变的独立相关因素包括：高龄 （OR 1.047,95%CI 1.026～1.069,P <0.0001）、吸烟（OR 1.887,95%CI 1.212～2.937,P =0.0050）、既 往缺血性脑血管病史（OR 2.260,95%CI 1.352～3.778,P =0.0019）和白质病变（OR 0.603,95%CI 0.394～0.922,P =0.0196）。颅内合并颅外动脉病变组独立相关因素包括：高龄（OR 1.022,95%CI 1.006～1.039,P =0.0064）、糖尿病（OR 1.494,95%CI 1.053～2.118,P =0.0244）和卒中家族史（OR 1.964,95%CI 1.302～2.961,P =0.013）。高同型半胱氨酸血症是3组共同的独立相关因素。 结论 颅内外动脉粥样硬化病变的相关因素可能存在差异。白细胞计数、空腹血糖、高密度脂蛋白 水平低与颅内动脉粥样硬化病变相关;高龄、吸烟、既往缺血性脑血管病史与颅外动脉粥样硬化相 关。高同型半胱氨酸血症是颅内外动脉病变的共同相关因素。     

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.     

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.     

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.     

Neonatal Seizures: Problems in Diagnosis and Classification

Summary: The clinical identification of neonatal seizures is critical for the recognition of brain dysfunction; however, diagnosis is often difficult because of the poorly organized and varied nature of these behaviors. Current classification systems are limited in their ability to communicate motor, autonomic, and electroencephalo-graphic features of seizures precisely and to provide a basis for uniform effective diagnosis, therapy, and determination of prognosis. Recent investigations of neonates, utilizing bedside electroencephalographic/polygraphic/ video monitoring techniques, have provided the basis for improved diagnosis and classification of seizures in the newborn. These studies have demonstrated that not all clinical phenomena currently considered to be seizures require electrocortical epileptiform activity for their initiation or elaboration. In addition, the specific clinical character of the phenomena considered to be seizures, the clinical state of the infant, and the character of the EEG indicate the probable pathophysiological mechanisms involved and suggest probable etiologies, prognosis, and therapy. Similarities between animal models that demonstrate reflex physiology and neonates with motor automatisms and tonic posturing suggest that these clinical behaviors may not be epileptic in origin but, rather, primitive movements of progression and posture mediated by brainstem mechanisms. Although not all clinical behaviors currently considered to be neonatal seizures may have similar pathophysiological mechanisms, they are clinically significant because they all indicate brain dysfunction.     

Valproate Monotherapy in the Management of Generalized and Partial Seizures

Summary: For decades, therapeutic tradition has promoted the concept of polypharmacy in the management of epilepsy. In recent years, however, studies have shown that, for most patients, monotherapy can provide comparable or better seizure control than administration of multiple anticonvulsants, while diminishing the potential for adverse reactions, drug interactions, and poor compliance. Valproate is an important monotherapeutic agent that is highly effective in the control of idiopathic primary and secondarily generalized epilepsies, and partial seizures that do not generalize. Comparative studies have found that valproate is at least as effective as phenytoin and carbamazepine in the treatment of generalized and partial seizures. Given the similar efficacy, other factors such as pharmacokinetics and side effects may therefore determine anticonvulsant selection for monotherapy.     

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.     

Un nouveau cadre conceptuel de travail pour la psychiatrie

In an attempt to place psychiatric thinking and the training of future psychiatrists more centrally into the context of modern biology, the author outlines the beginnings of a new intellectual framework for psychiatry that derives from current biological thinking about the relationship of mind to brain. The purpose of this framework is twofold. First, it is designed to emphasize that the professional requirements for future psychiatrists will demand a greater knowledge of the structure and functioning of the brain than is currently available in most training programs. Second, it is designed to illustrate that the unique domain which psychiatry occupies within academic medicine, the analysis of the interaction between social and biological determinants of behavior, can best be studied by also having a full understanding of the biological components of behavior.