阿替普酶辅助颅内血肿微创手术在中等量基底节区脑出血治疗中的临床疗效

目的探讨阿替普酶辅助颅内血肿微创手术对基底节区中等量脑出血临床疗效和安全评估。方法选取我院从2012年1月~2016年7月收治的GCS评分8~10分的基底节区中等量脑出血患者63例,分为实验组和对照组,实验组进行阿替普酶辅助颅内血肿微创手术治疗,对照组给予内科保守治疗。通过GCS、NIHSS、日常生活活动能力量表(ADL)及mRS量表评价两组患者治疗效果,并进行比较。结果两组患者出血量在治疗前无明显差异;出院时复查CT显示,实验组治疗后血肿几乎全部清楚或吸收,对照组血肿量无明显减少,两组之间具有统计学意义(P0.05)。实验组治疗后NIHSS评分较治疗前明显下降(P0.05),而对照组治疗前后变化无明显统计学差异。实验组治疗后GCS评分较治疗前明显增加(P0.05)。出院3个月后实验组患者的ADL评分较对照组明显增加(P0.05),mRS评分较对照组明显降低(P0.05)。结论阿替普酶辅助颅内血肿微创手术治疗基底节区脑出血能更快清除颅内血肿,减轻血肿压迫造成的脑损伤,从而减少患者致残率和死亡率,安全有效。     

超早期强化降压治疗对脑出血血肿扩大神经功能及预后的影响

目的探讨超早期强化降压治疗对脑出血血肿扩大、神经功能及预后的影响。方法回顾性分析选择2013-01—2015-10在我科治疗的162例脑出血患者的临床资料。其中71例患者在超早期进行了强化降压为研究组,91例患者给予常规降压为对照组。比较2组患者治疗后血压控制情况、血肿扩大发生率、NIHSS评分、随访Rankin评分。结果治疗后1h及24h,研究组收缩压显著低于对照组,差异有统计学意义(P0.01)。治疗后24h,研究组NIHSS评分显著低于对照组,差异有统计学意义(P0.01)。治疗后90d随访,研究组患者Rankin评分为0~2分的比例显著高于对照组,差异有统计学意义(P0.05)。治疗后24h,研究组血肿量、血肿扩大发生率均显著低于对照组,差异有统计学意义(P0.05)。结论超早期强化降压治疗能够缓解脑出血血肿扩大情况,改善神经功能,改善预后。     

奥拉西坦治疗高血压脑出血52例疗效观察

目的 探讨奥拉西坦对高血压脑出血患者的临床治疗价值.方法 将2010-05-2011-09我科收治的高血压脑出血患者104例随机分为对照组、观察组各52例,对照组仅接受常规治疗,观察组在常规治疗的基础上再给予奥拉西坦,对比分析2组治疗前后Barthel指数、简易精神状态量表（MMSE）评分、美国国立卫生研究院卒中量表（NIHSS）评分的变化幅度.结果 治疗后,所有患者的Barthel指数、MMSE评分均显著升高,NIHSS评分显著下降,治疗前后相比差异有统计学意义（P＜0.05）.但观察组的Barthel指数、MMSE评分升高幅度显著大于对照组,NIHSS评分降低幅度显著大于对照组,2组比较差异有统计学意义（P＜0.05）.结论 奥拉西坦可显著改善高血压脑出血患者的认知功能障碍问题,可作为高血压脑出血的常规治疗药物之一.     

“梯度减压”联合甘露醇在高血压脑出血微创血肿清除术患者中的实践研究

目的探讨"梯度减压"联合甘露醇在高血压脑出血微创血肿清除术患者中的实践效果。方法选取2016年3月～2019年4月本院收治的高血压脑出血患者93例,随机分为对照组(46例)与观察组(47例)。对照组给予微创血肿清除术及甘露醇治疗,观察组给予梯度减压、微创血肿清除术及甘露醇治疗。对比术中及术后并发症(脑膨出、迟发性血肿、脑梗死等)发生情况,另对比术前、术后7 d及术后14 d的美国国立卫生研究院卒中量表(NIHSS)评分及术后6个月格拉斯哥预后量表(GOS)评分情况。结果观察组术中脑膨出发生率及总并发症发生率均低于对照组,差异明显(P0.05);NIHSS评分在组间、时间、交互方面具有明显差异(P0.05),2组术后7 d及术后14 d的NIHSS评分均低于术前,2组术后14 d均低于术后7 d,观察组术后7 d、术后14 d的NIHSS评分均低于对照组,均有明显差异(P0.05);2组术后6个月GOS评分等级分布比较差异有统计学意义(P0.05),观察组(Ⅴ+Ⅳ)级占比高于对照组,差异明显(P0.05)。结论在高血压脑出血微创血肿清除术患者中应用"梯度减压"联合甘露醇治疗,可明显减少脑膨出等并发症发生,促进神经功能恢复,改善预后。     

rt-PA静脉溶栓治疗不同时间窗椎-基底动脉系统脑梗死的临床疗效观察

目的探讨椎-基底动脉系统脑梗死患者不同时间窗重组组织型纤溶酶原激活剂(recombinant tissue plasminogen activator,rt-PA)静脉溶栓治疗的临床疗效。方法回顾性分析50例椎-基底动脉系统脑梗死患者临床资料,按溶栓治疗时间窗分为4.5 h组和4.5~9 h组,每组25例。比较两组患者神经功能缺损量表(national institutes of health stroke scale,NIHSS)评分、Barthel指数(Barthel index,BI)评分、改良Rankin量表(modified Rankin scale,mRS)评分及脑出血发生率。结果与治疗前相比较,治疗后14 d、30 d、90 d时4.5 h组和4.5~9 h组NIHSS评分和BI评分均显著升高,组间比较差异显著(P0.05)。治疗前及治疗后14 d、30 d、90 d,两组患者NIHSS评分和BI评分比较均无统计学差异(P0.05)。治疗后90 d,两组患者mRS评分比较无统计学差异(P0.05)。4.5 h组和4.5~9 h组BI评分脑出血发生率分别为4.0%(1/25)、8.0%(2/25),组间比较差异无统计学意义。结论椎-基底动脉系统脑梗死患者发病9 h内应用rt-PA静脉溶栓治疗是安全有效的。     

前列腺素E1对高血压脑出血患者血肿周围组织血流量及预后的影响

目的 观察前列腺素(PG)E1对高血压脑出血患者血肿周围组织血流量及预后的影响.方法 40例高血压脑出血患者随机分为PGE1组和对照组,两组患者均给予脑出血的常规治疗;PGE1组发病后第5d起给予PGE1治疗15 d.发病后第5 d、20 d进行单光子发射计算机断层扫描脑灌注显像,应用半定量分析法计算血肿区及血肿周围组织近区、远区及额顶叶区的局部脑血流量(rCBF);发病第1d、第5 d、第12 d和第20 d进行头颅CT检查,观察两组患者血肿及血肿周围低密度区体积;同时应用美国国立卫生研究院卒中量表(NIHSS)进行神经功能缺损程度评分;发病第1 d、第20 d进行改良的Rankin量表(mRS)评分,第90 d时再次分别进行NIHSS和mRS评分.结果 发病第20 d PGE1组血肿周围近区及远区rCBF较治疗前及对照组明显升高(均P<0.01);发病第12 d、20 d时血肿体积以及发病第20 d时血肿周围低密度区较对照组明显缩小(均P<0.01);发病第20 d和第90 d时NIHSS评分较对照组明显降低(均P<0.05);发病第90d时mRS评分较对照组明显降低(P<0.01).结论 高血压脑出血患者应用PGEI治疗,可增加血肿周围rCBF,促进神经功能缺损的恢复,改善预后.     

阿替普酶静脉溶栓治疗急性脑梗死的疗效及安全性

目的研究重组组织型纤溶酶原激活物(rt-PA)静脉给药溶栓治疗急性脑梗死的临床效果。方法回顾性分析发病在4.5h内,具有溶栓指征的急性脑梗死患者105例,其中对照组56例仅给予抗血小板聚集、调脂稳定斑块等常规治疗方案,观察组49例给予rt-PA静脉溶栓治疗,24h后若无明显出血,开始给予脑梗死常规治疗。比较2组治疗后90d美国国立卫生院卒中量表(NIHSS)评分、Barthel指数(BI)评分及改良Rankin量表(mRS)评分改善情况,以评价rt-PA治疗急性脑梗死临床疗效。结果 2组治疗前NIHSS评分差异无统计学意义(P0.05),观察组溶栓后2h、24h、7d时NIHSS评分显著低于对照组(P0.05);观察组90d时mRS评分显示预后良好的患者较对照组明显增多,2组比较差异有统计学意义(P0.05);与对照组比较,观察组90d时Barthel指数评分明显升高(P0.05)。虽然观察组总体出血事件较对照组增高(P0.05);但2组症状性脑出血比较差异无统计学意义(P0.05)。结论发病4.5h以内,静脉给予rt-PA溶栓治疗急性脑梗死具有显著的临床疗效,且安全性较高,值得临床推广应用。     

不同时间窗rt-PA静脉溶栓治疗椎-基底动脉系统脑梗死的疗效观察

目的探讨不同时间窗rt-PA静脉溶栓治疗椎-基底动脉系统脑梗死的临床疗效。方法选取2016年8月~2017年8月我院收治的70例椎-基底动脉系统脑梗死患者为研究对象,所有患者均经多模式MRI证实且行rt-PA静脉溶栓治疗,根据患者溶栓治疗时间窗不同,将其分为4.5 h组(35例)和4.5~9 h组(35例),比较两组神经功能缺损量表(national institutes of health stroke scale,NIHSS)评分、Barthel指数(Barthel index,BI)评分及改良Rankin量表(modified Rankin scale,mRS)评分,观察两组脑出血发生情况。结果与治疗前比较,4.5 h组和4.5~9 h组患者溶栓后24 h、14 d、30 d及90 d的NIHSS评分显著降低(P0.05),BI评分显著升高(P0.05),而两组患者在rt-PA静脉溶栓治疗后的NIHSS评分及BI评分比较,差异无统计学意义(P0.05);两组rtPA静脉溶栓后90 d的mRS评分及预后良好率比较均无明显差异(P0.05)。3 m随访期内,4.5 h组脑出血发生率为5.71%,4.5~9 h组脑出血发生率为8.57%,两组比较差异无统计学意义(P0.05)。结论 I扩大时间窗至9 h对椎-基底动脉系统脑梗死行rt-PA静脉溶栓治疗安全有效,因此,对于治疗时间窗为4.5 h~9 h的椎-基底动脉系统脑梗死也可行rt-PA静脉溶栓治疗。     

自体骨髓间充质干细胞移植辅助高压氧治疗高血压脑出血临床观察

目的：观察自体骨髓间充质干细胞移植辅助高压氧治疗高血压脑出血的疗效。方法将102例高血压脑出血患者随机分为治疗组（自体骨髓间充质干细胞移植＋高压氧治疗组）和对照组（高压氧治疗组）,比较2组患者治疗前和治疗后6个月的神经功能缺损程度评分（NIHSS）和日常生活活动能力评分（Barthel指数）,治疗后6个月格拉斯哥预后评分（GOS）及远期生活质量评估量表评分（KPS）。结果治疗后6个月与对照组比较,NIHSS评分均有显著降低Barthel指数均有显著升高（P＜0·05）,治疗组GOS及KPS评分显著好于对照组（P＜0·05）。结论自体骨髓间充质干细胞移植辅助高压氧治疗能显著促进高血压脑出血患者神经功能恢复,提高患者生存率和生活质量。     

尤瑞克林联合丹红治疗急性脑梗死的疗效观察

目的 观察尤瑞克林联合丹红注射液治疗急性脑梗死的有效性,为脑梗死急性期的治疗提供临床参考。方法 选择2017-12—2019-12郑州大学第二附属医院收治的120例急性脑梗死患者,实验组及对照组各60例,在脑梗死常规治疗的基础上,对照组应用丹红,实验组在丹红的基础上加用尤瑞克林,比较2组患者在入院后2周及1个月的NIHSS评分及Barthel指数,从而评估其药物有效性。结果 实验组及对照组患者入院后2周及1个月的NIHSS评分Barthel指数比较:(1)入院后2周,2组NIHSS评分分别为(5.33±3.79)分及(6.20±4.68)分,Barthel指数分别为(55.92±19.45)分及(52.58±26.17)分,实验组NIHSS评分稍低于对照组,其Barthel指数稍高于对照组,但其差异无统计学意义(P0.05);(2)入院后1个月,2组NIHSS评分分别为(3.52±2.94)分及(5.17±4.11)分,Barthel指数分别为(67.00±17.33)分及(56.17±25.49)分,实验组NIHSS评分显著低于对照组,Barthel指数显著高于对照组,其差异具有统计学意义(P0.05)。结论 应用尤瑞克林联合丹红注射液治疗14d,可显著改善急性脑梗死患者1个月后的神经功能缺损症状,并提高其日常生活能力。     

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.     

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.     

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.     

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.     

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.     

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.