急性缺血性脑卒中血管介入治疗方法和装置的研究进展

机械血栓切除术可治疗伴大血管闭塞的前循环和后循环急性缺血性脑卒中。机械血栓切除术失败后仍应进行支架植入术;接触抽吸术与支架取栓术的优劣难分仲伯;伴大血管闭塞的动脉粥样硬化性前循环急性缺血性脑卒中,血管成形术和(或)支架置入术要优于支架取栓术;支架取栓术加动脉内溶栓治疗有叠加效应,但机械血栓切除术加静脉溶栓则无叠加效应;远程缺血预处理和替罗非班有减少手术并发症的功效;紫杉醇洗脱支架和新型支架是值得推广的新型血管内治疗装置。     

急性缺血性卒中大血管闭塞性质的判断与取栓方式和材料的选择

血管内机械取栓是治疗大血管闭塞性急性缺血性卒中的有效治疗方法。应结合病史、发 病形式及影像学检查等综合判断病变性质；依据病变性质并参考手术路径，个性化选择支架取栓、 抽吸取栓、球囊/支架血管成形术、动脉溶栓任一种或多种方法联合取栓；并依据手术方式选择手 术材料，以快速高效地完成手术。     

急性基底动脉闭塞的治疗进展

【摘要】 基底动脉闭塞病情重,致死率和致残率高,静脉溶栓、动脉溶栓治疗和机械取栓治疗是目前最常见的治疗方法。与静脉溶栓相比,动脉溶栓或机械取栓治疗血管再通率较高,且时间窗较静脉溶栓治疗宽,但目前的研究并未证实动脉溶栓或机械取栓治疗优于静脉溶栓治疗。桥接治疗是结合静脉溶栓与动脉溶栓或机械取栓的具有发展前景的一种治疗新模式,但其有效性还需要进一步证实。本文将对急性基底动脉闭塞相关的治疗方法：静脉溶栓、动脉溶栓、机械取栓治疗等做一综述,以促进对急性基底动脉闭塞血管再通治疗的认识。     

急性缺血性脑卒中血管内治疗21例临床分析

目的探讨急性缺血性脑卒中血管内治疗的方法、疗效和安全性。方法回顾性分析血管内治疗的大血管闭塞的急性缺血性脑卒中患者21例。10例为阿替普酶静脉溶栓后桥接血管内治疗,11例直接行血管内治疗。其中机械取栓12例,机械取栓+支架植入3例,单纯颈动脉支架植入3例,机械取栓+动脉溶栓1例,机械取栓+动脉溶栓+支架植入1例,单纯动脉溶栓1例。评估术中mTICI再通等级、并发症及术后随访第90天m RS评分,分析疗效与安全性。结果21例患者前循环卒中18例,后循环卒中3例。NIHSS评分平均15. 81±6. 44分。20例患者术后血管再通达mTICI 2 b-3级。术中并发出血1例,术后大量颅内出血1例,无症状少量颅内出血4例。术后高灌注综合征8例,其中4例行去骨瓣减压术,最终死亡5例(23. 81%)。术后随访第90天mRS评分0～2分8例。结论经充分评估并及时采取适宜的单一或多种血管内治疗方法对于大血管闭塞导致的急性缺血性脑卒中患者安全有效。     

急性缺血性脑卒中血栓组织学及对临床干预影响的研究进展

急性缺血性脑卒中是临床上常见的脑血管病，系血栓阻塞颅内动脉导致脑功能障碍，具有发病率高、致残率高、复发率高及并发症多等特点，目前临床干预主要采取溶栓和取栓治疗。研究表明，血栓的组成与结构影响溶栓、取栓疗效，本文就脑血栓组织学及其对溶栓、取栓影响有关研究进行综述，为临床治疗方案的选择提供参考。     

急性缺血性卒中大血管闭塞性质的判断与取栓方式和材料的选择

血管内机械取栓是治疗大血管闭塞性急性缺血性卒中的有效治疗方法。应结合病史、发
病形式及影像学检查等综合判断病变性质；依据病变性质并参考手术路径，个性化选择支架取栓、
抽吸取栓、球囊/支架血管成形术、动脉溶栓任一种或多种方法联合取栓；并依据手术方式选择手
术材料，以快速高效地完成手术。     

急性缺血性脑卒中机械取栓治疗的并发症分析

正2015年急性缺血性脑卒中介入治疗终于迎来了发展的"春天",中美两国卒中学会相继发布消息,将机械取栓以最高等级推荐用于急性缺血性脑卒中患者的救治~([1-2])。虽然发表于新英格兰杂志的著名MR CLEAN~([3])、ESCAPE~([4])、EXTEND-IA~([5])、SWIFT PRIME~([6])等临床试验结果提示血管内支架取栓能够显著改善急性缺血性脑卒中患者预后,且较过去传统的静脉溶栓治疗方法比较,机械取栓治疗时间窗显著延长,血管开通率显著提高,已显示出较大的应用前景。但由     

Solitaire支架血管内机械取栓治疗急性大脑中动脉闭塞效果分析

目的探讨Solitaire支架血管内机械取栓治疗急性大脑中动脉闭塞致缺血性卒中的有效性和安全性,并筛查影响预后的相关因素。方法共25例急性大脑中动脉M1段闭塞致缺血性卒中患者均采用Solitaire支架血管内机械取栓,记录发病至股动脉穿刺时间、股动脉穿刺至血管再通时间、血管内机械取栓次数、取栓前是否静脉溶栓、是否行球囊扩张术和(或)支架植入术、取栓后是否动脉溶栓、术后是否应用替罗非班;术后即刻采用脑梗死溶栓血流分级(TICI)评价血管再通情况,术后24 h采用美国国立卫生研究院卒中量表(NIHSS)评价神经功能,术后90 d采用改良Rankin量表(mRS)评价临床预后;记录术后24 h症状性颅内出血发生率和术后90 d内病死率。结果 25例患者发病至股动脉穿刺中位时间5.00(4.00,6.30)h,股动脉穿刺至血管再通中位时间2.00(2.00,2.50)h,血管内机械取栓次数2(2,2)次,7例(28%)先行静脉溶栓再桥接血管内机械取栓,6例(24%)行单纯球囊扩张术,3例(12%)行单纯支架植入术,4例(16%)行球囊扩张术和支架植入术,4例(16%)取栓后行动脉溶栓,11例(44%)术后应用替罗非班;20例(80%)血管再通(TICI分级2b~3级);术后24 h NIHSS评分低于入院时[8(4,12)分对14(11,17)分;Z=-3.532,P=0.000],3例(12%)发生症状性颅内出血;术后90 d 15例(60%)预后良好(mRS评分≤2分),2例(8%)死亡。单因素和多因素前进法Logistic回归分析显示,TICI分级2b~3级是血管内机械取栓预后良好的独立因素(OR=0.316,95%CI:0.102~0.982;P=0.046)。结论 Solitair支架血管内机械取栓治疗急性大脑中动脉闭塞致缺血性卒中安全、有效,且大脑中动脉再通级别越高、预后越佳。     

经微导管机械碎栓和SolitaireAB型支架取栓治疗急性缺血性脑卒中的比较研究

目的比较经微导管机械碎栓和SolitaireAB支架取栓两种方法治疗急性缺血性脑卒中的疗效及安全性。方法回顾性分析2014年1月至2015年12月本院神经内科收治的78例急性脑动脉栓塞患者病历资料,根据治疗方案不同分为A、B两组各39例,A组应用血管内经微导管机械碎栓联合接触性动脉溶栓治疗,B组应用SolitaieAB型支架取栓联合尿激酶溶栓治疗,比较两组患者术后3天、30天脑卒中量表(NIHSS)评分、血管再通率及并发症发生率。结果两组患者术后3天、30天NIHSS评分均较术前显著降低,A组术后3天NIHSS评分显著高于B组(6.0±1.6vs.5.2±1.3)(P0.05),术后30天两组NIHSS评分差异无统计学意义(3.5±1.8vs.3.3±1.5)(P0.05);B组术后3天(92.3%vs.79.5%)、30天(97.4%vs.92.3%)血管再通率均高于A组,但差异无统计学意义(P0.05);两组术后并发症发生率(10.2%vs7.7%)差异亦无统计学意义。结论支架内取栓治疗急性缺血性脑卒中短期疗效略优于经微导管机械碎栓;术后联合尿激酶溶栓,两者恢复期疗效相近。     

抽吸取栓与支架取栓在急性缺血性卒中治疗中的研究进展

急性缺血性卒中血管内治疗是静脉溶栓后又一血管再通疗法，一线治疗技术为支架取栓， 抽吸取栓是相对支架取栓的另一种技术。文章对抽吸取栓与支架取栓在急性缺血性卒中患者血管 内治疗中的疗效进行综述。急性缺血性卒中血管内治疗目前仍以支架取栓作为一线技术，作为补充 技术的抽吸取栓从股动脉穿刺到再灌注的时间较短，未来研究可能更着重于按特定部位或病因采 取不同的取栓技术。     

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.     

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.     

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.     

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.     

The influence of comorbid depression on seizure severity

PURPOSE: To determine the relation between depressive symptoms and seizure severity among people with epilepsy. METHODS: A postal questionnaire was used to survey a nationwide community sample about seizures and depression. The Seizure Severity Questionnaire (SSQ) assessed the severity and bothersomeness of seizure components. The Centers for Epidemiological Studies-Depression scale categorized levels of depression. RESULTS: Respondents categorized as having current severe (SEV, n = 166), mild-moderate (MOD, n = 74), or no depression (NO, n = 443) differed significantly in SSQ scores (all p < 0.0001). People with SEV or MOD reported significantly worse problems than did those with NO depression for overall seizure recovery (mean, 5.3, 4.9, 4.5, respectively); overall severity (5.0, 4.5, 4.2); and overall seizure bother (5.3, 4.8, 4.4) (all p < 0.005). Cognitive, emotional, and physical aspects of seizure recovery also were rated worse among people with SEV than with NO depression (all p < 0.05). Symptoms of depression were significantly correlated with higher levels of all components of generalized tonic-clonic seizure severity (r = 0.33-0.48; all p < 0.0001), and partial seizures (r = 0.31-0.38; all p < 0.01). CONCLUSIONS: Clinically depressed people with epilepsy reported higher levels of perceived severity and bother from seizures, as well as greater problems with overall seizure recovery than did nondepressed people experiencing similar types of seizures. The pervasive influence of depressive symptoms on reports of seizure activity suggests that people with epilepsy should be screened for depression. These data highlight the importance of detecting and treating depression among people with epilepsy.     

Dextromethorphan: Cellular Effects Reducing Neuronal Hyperactivity

Summary: Dextromethorphan is a dextrorotary morphinan without affinity for opioid receptors, commonly used as an antitussive medication. During the past 5 years, interest in the compound and its demethylated derivative, dextrorphan, has been revived because additional neuroprotective and an-tiepileptic properties were found in in vitro studies, animal experiments, and a few clinical cases. Both morphinans are able to inhibit N -methyl-D-aspartate (NMDA) receptor channels and voltage-operated calcium and sodium channels with different potencies. The inhibition of the NMDA receptor is believed to be the predominant mechanism of action responsible for the anticonvulsant and neuroprotective properties of the compounds.