短暂性脑缺血发作后发生脑梗死风险的预测研究

目的 探讨ABCD2评分和ABCD2评分结合MRI弥散加权成像(DWI)和颅内动脉MR血管成像(MRA)对短暂性脑缺血发作(TIA)后脑梗死的预测价值.方法 分别采用ABCD2评分及ABCD2+ DWI+MRA评分对182例TIA患者进行评定,观察TIA后2d、7d和30 d内的脑梗死发生率.采用ROC曲线评估ABCD2及ABCD2+ DWI+ MRA评分对TIA后脑梗死风险的预测准确度.结果 本组56例(30.8％)患者于30 d内发生脑梗死,其中42例(23.1％)发生于7d内,19例(10.4％)发生于2d内,均无脑出血发生.与低危组比较,中危组与高危组各时间点脑梗死发生率显著升高(均P＜0.05).DWI异常患者各时间点脑梗死发生率明显高于正常者(均P＜0.05).30 d时颅内动脉狭窄≥50％的患者脑梗死发生率明显高于颈内动脉狭窄＜50％的患者(P＜0.05).伴DWI异常及颅内动脉狭窄≥50％的低危组患者各时间点脑梗死发生率显著高于DWI正常和颅内动脉狭窄＜50％的患者(均P＜0.05).ABCD2+ DWI+ MRA评分预测TIA第2d、第7d及第30 d的脑梗死率的曲线下面积显著高于ABCD2评分(均P＜0.001).结论 ABCD2评分结合DWI和MRA能进一步提高预测TIA后发生脑梗死的准确性.     

ABCD2评分法结合CTA预测TIA患者近期卒中风险的临床研究

目的 探讨采用ABCD2评分法对短暂脑缺血发作(TIA)患者短期内进展为脑梗死的预测价值;评价脑血管狭窄与TIA患者脑梗死发生率及ABCD2评分之间的关系.方法 按照Johnston等对TIA的ABCD2评分标准,测定98例TIA患者的评分并危险分组,观察其2、7d内脑梗死的发生率,比较各危险组之间卒中率的差异;通过CTA评估脑血管狭窄,并分为血管狭窄≥50％组与血管狭窄＜50％组,分析脑血管狭窄与2、7d内脑梗死的发生率的关系,评价ABCD2评分与脑血管狭窄之间的相关性.结果 (1)评分≤3分的TIA患者有40例.2、7d发生脑梗死的例数分别为0例(0％)、2例(5％);评分为4～5分的患者46例,2、7d进展为脑梗死的例数分别为4例(8.7％)、11例(23％);评分≥6分的患者12例,2、7d进展为脑梗死的例数分别为3例(25％)、4例(33.3％).不同ABCD2评分值的TIA患者,其脑梗死发生率差异均有统计学意义(P均＜0.05).(2)脑血管狭窄≥50％组与狭窄＜50％组比较,TIA后7d内卒中发生率明显增高,且其脑梗死发生率差异有统计学意义(21.4％ vs 5.6％,P=0.04).(3)血管狭窄≥50％组与狭窄＜50％组比较,中、高危的比率增高(46.4％ vs 19.4％),且其比率增高有统计学意义(P=0.02).结论 (1) ABCD2评分能够预测TIA患者2、7d内卒中发生率,是临床预测TIA短期进展为脑梗死的一种简便、有效的方法.ABCD2评分值不同的TIA患者,脑梗死的发生率不同,分值越高,发生率越高.(2)合并中重度血管狭窄的TIA患者较脑血管无明显狭窄的TIA患者更易发生脑梗死.(3)ABCD2评分与脑血管狭窄具有相关性.     

ABCD2评分及责任血管狭窄对短暂性脑缺血发作进展为脑梗死的预测价值

目的 探讨ABCD2评分与责任血管狭窄对短暂性脑缺血发作(TIA)后脑梗死发生的预测价值. 方法 将焦作市人民医院神经内科自2008年至2011年收治的93例TIA患者根据ABCD2评分分为低危组(20例)、中危组(48例)、高危组(25例),并行DSA检查,根据责任血管狭窄程度分为正常或轻度狭窄(狭窄率＜50％)、中度狭窄(狭窄率50％～69％)、重度狭窄(狭窄率70％～100％).根据Logistic β回归系数分别对ABCD2评分及责任血管狭窄程度进行危险因素赋分,通过线性函数转换建立危险评分系统. 结果 发病7d内低危组脑梗死发生率为5.0％,中危组为10.4％,高危组为36.0％;中、低危组的脑梗死率发生率均明显低于高危组,差异有统计学意义(P＜0.05).65例(69.9％)患者有不同程度的责任血管狭窄或闭塞,其中正常或轻度狭窄54例、中度狭窄22例及重度狭窄17例;中度狭窄组及重度狭窄组脑梗死发生率(27.3％、47.1％)均明显高于正常或轻度狭窄组(1.9％),差异有统计学意义(P＜0.05).基于入院危险因素建立的预测模型性能良好(拟合优度检验P＞0.05,C统计值为0.887).利用危险评分系统成功地将TIA患者分为低危、中危和高危脑梗死组,模型建立数据中患者进展性脑梗死发生率分别为1.9％、25.0％和47.1％. 结论 ABCD2评分及责任血管狭窄程度对TIA患者进展为脑梗死的预测有重要意义.根据ABCD2评分及责任血管狭窄程度建立的预测模型可以早期、方便、准确地预测TIA后脑梗死的发生,开发的预测工具可辅助临床决策的制定.     

颈内动脉系统短暂性脑缺血发作患者颅内血管狭窄程度和ABCD2评分与近期预后的关系

目的探讨颈内动脉系统短暂性脑缺血发作(TIA)患者颅内血管狭窄和ABCD2评分与近期预后的关系。方法对64例颈内动脉系统TIA患者行MRI、MR血管成像(MRA)检查及ABCD2评分,并分析其与近期预后的关系。结果 MRA结果显示,47例(73.4%)患者有不同程度的颅内血管狭窄或闭塞,其中正常或轻度狭窄组37例,中度狭窄组16例及重度狭窄组11例;根据ABCD2评分结果,低危组22例,中-高危组42例。发病7 d内14例(21.9%)发生脑梗死,中度狭窄组(12.5%)及重度狭窄组(7.81%)脑梗死发生率显著高于正常及轻度血管狭窄组(1.6%)(均P<0.05)。中-高危组中重度血管狭窄率及脑梗死发生率显著高于低危组(均P<0.05)。结论颈内动脉系统TIA患者颅内血管狭窄程度及ABCD2评分对TIA的近期预后评估有重要的意义。     

ABCD2评分对短暂性脑缺血发作患者发生脑梗死风险的评估价值

目的探讨ABCD2评分对短暂性脑缺血发作(TIA)患者发生脑梗死风险的评估价值。方法对病程<7 d的220例TIA患者应用ABCD2评分分为低危组(0～3分)和中-高危组(4～7分),观察并比较两组患者TIA发病7 d、6个月、1年内脑梗死的发生率。结果根据ABCD2评分,108例患者归为低危组,112例归为中-高危组。TIA发病7 d、6个月及1年内低危组脑梗死发生率分别为4.6%、6.5%及7.4%,中-高危组脑梗死发生率分别为18.8%、27.7%及33.9%;中-高危组TIA发病7 d、6个月及1年内脑梗死发生率显著高于低危组(均P<0.05)。结论 ABCD2评分是临床上预测TIA患者发生脑梗死的有效方法。     

ABCD~3-I评分法和纤维蛋白原水平预测TIA后短期脑梗死风险的临床价值

目的探讨ABCD3-I评分法结合纤维蛋水平白原检测对短暂性脑缺血发作(TIA,Transient ischemic attack)短期发生脑梗死的风险进行评估。方法用ABCD3-I评分法和ABCD~3-I评分法+纤维蛋白原水平分别测定200例TIA患者的评分,并观察TIA后7d内脑梗死的发生率。结果 200例TIA患者中7d内发生脑梗死的有27例。ABCD3-I评分组中低危组(0～3分)、中危组(4～7分)、高危组(8～13分)TIA患者7d内脑梗死发生率分别为3.23%、11.63%和29.27%(P0.05),ABCD3-I评分+Fib水平组中低危组(0～3分)、中危组(4～7分)、高危组(8～13分)TIA患者7d内脑梗死发生率分别为3.23%、9.92%和30.61%(P0.05)。ABCD3-I评分法和ABCD3-I评分法+纤维蛋白原水平检测的ROC曲线下面积(95%CI)分别为0.66(0.56～0.77)和0.69 (0.59～0.80)。ABCD3-I评分法和ABCD~3-I评分法+纤维蛋白原水平组的评分与脑梗死发生率呈线性相关,相关系数分别为0.23、0.26(P0.05)。结论 ABCD3-I评分能够较为准确地对TIA患者7d内发生缺血性脑梗死的风险进行预测,结合纤维蛋白原水平检测更能为准确地预测脑梗死的发生风险。     

ABCD2评分结合头颈CTA对短暂性脑缺血发作后近期发生脑梗死的评估价值

目的：分析ABCD2评分结合头颈CT血管成像（CTA）表现对短暂性脑缺血发作（TIA）后7 d患者发生脑梗死的评估价值。方法：以2008年12月至2011年3月住院的120例TIA患者为研究对象,收集相关资料并进行率的χ2检验。结果：31/120例（25.83%）患者在TIA后7 d内发生脑梗死。ABCD2评分≥6分为高危组,ABCD2评分4~5分为中危组,ABCD2评分≤3分为低危组。TIA后7 d脑梗死发生率,CTA颅内外动脉狭窄≥50%的患者中与〈50%的患者相比明显增高（P〈0.01）。结论：ABCD2评分法预测7 d发生脑梗死风险的准确性较高,进一步结合CTA检查能提高预测的准确性。     

短暂性脑缺血发作后短期内发生脑梗死的风险分析

目的分析ABCD2评分结合MRA对短暂性脑缺血发作(TIA)后7~30d脑梗死发生的评估价值。方法以2008年12月~2009年10月住院的TIA患者为研究对象,收集其临床资料和磁共振血管成像(MRA)检查结果,按Johnston提出的7分"ABCD2"评分法给予评分,随访TIA后7d和30d内脑梗死的发生率,并分析"AB-CD2"评分、MRA与TIA后短期内发生脑梗死的关系。结果 50例(42.0%)TIA患者于30d内发生脑梗死,其中29例(24.4%)发生于7d内;"ABCD2"评分与TIA后7d和30d脑梗死发生率之间呈直线相关,"ABCD2"评分越高,脑梗死的发生率越高(P0.001);TIA后7d和30d颅内动脉狭窄≥50%的患者中脑梗死发生率比50%的患者明显增高(P0.05)。结论 "ABCD2"评分法对TIA后脑梗死发生有预测价值,"ABCD2"评分结合MRA检查能进一步提高预测的准确性。     

ABCD~2评分结合经颅多普勒和颈部血管超声对TIA患者近期预后的评价

目的分析ABCD2评分结合经颅多普勒和颈部血管超声对短暂性脑缺血发作(TIA)后7 d发生脑梗死的评估价值。方法以2010年1月～2011年1月住院治疗的126例TIA患者作为研究对象,收集其临床、TCD和颈部血管超声检查资料。按ABCD2评分法进行评分,计算TIA后7 d内脑梗死发生率。结果 126例TIA患者7 d内进展为脑梗死者26例,占20.6%。ABCD2评分越高,脑梗死的发生率越高(P<0.05)。TIA后7 d脑供血动脉狭窄≥50%的患者中脑梗死发生率较脑供血动脉狭窄<50%的患者明显升高(P<0.05)。ABCD2评分≥4分、脑供血动脉狭窄≥50%的TIA患者7 d脑梗死发生率为33.8%,与ABCD2评分≥4分、脑供血动脉狭窄<50%的TIA患者(7.7%)比较,其发生脑梗死的风险明显增加(P<0.05)。结论 ABCD2评分法预测7 d发生脑梗死风险的准确性较高,进一步结合经颅多普勒和颈部血管超声检查可提高预测的准确性。     

改良ABCD2评分与头颈部CTA对TIA后脑梗死的预测价值

目的 探讨应用改良ABCD2 评分及头颈部CT血管造影（CTA）对短暂性脑缺血发作（TIA）后7 d内脑梗死发生率的预测价值,并分析改良ABCD2评分及CTA的相关性。方法 回顾性分析698例TIA的临床资料及CTA资料。采用ABCD2评分法进行评分的同时,附加人血浆脂蛋白相关磷脂酶A2（Lp-PLA2）检测结果进行评分,分为低危组、中危组、高危组;根据头颈CTA血管狭窄程度分为正常或轻度狭窄、中度狭窄及重度狭窄。结果 698例TIA中,7 d内166例发生脑梗死;低危组、中危组及高危组脑梗死发生率呈现递增趋势（P<0.05）。责任血管重度狭窄组7 d内脑梗死发生率明显高于中度狭窄组（P<0.05）,而中度狭窄组明显高于正常或轻度狭窄组（>P<0.05）。低危组、中危组及高危组责任血管重度狭窄率、多支血管病变比例均呈现递增趋势（>P<0.05）,而3组病变血管位于前循环比例无统计学差异（>P>0.05）。结论 应用改良后ABCD2评分及CTA检查对TIA的脑梗死风险预测均有重要意义。     

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.