甘露醇治疗大面积脑梗死临床分析

目的观察大面积脑梗死患者脑脊液中甘露醇的含量变化。方法 50例大面积脑梗死患者,用可见-紫外分光光度计测定血清及脑脊液中甘露醇含量。结果 （1）血清中甘露醇10h排出达97%。（2）脑脊液中甘露醇含量逐日增加,第7天达1 387μg/mL。结论甘露醇可通过血脑屏障进入脑脊液中,大面积脑梗死患者甘露醇输入不宜超过7d。     

脑出血患者血肿周围水肿形成机制:脑内细胞因子的作用

目的 :探讨脑出血患者脑内炎性细胞因子与血肿周围水肿的形成是否相关。方法 :32例脑出血患者行血肿清除术后 ,留取脑血肿液 ,放免法测定其中肿瘤坏死因子α(TNFα)和白细胞介素 - 6 (IL - 6 )的含量 ,测量术前检查的头 CT上的血肿周围水肿带大小 ,用 SPSS10 0对两者进行相关分析。结果 :脑出血患者脑血肿液中 IL - 6和 TNFα的含量明显高于正常人溶血血清中的含量 (P<0 .0 1) ;脑血肿液中 TNFα和 IL - 6含量与血肿周围水肿带大小呈正相关 (r TNF=0 .5 39,P<0 .0 1;r IL- 6 =0 .5 6 9,P<0 .0 1)。结论 :脑出血患者急性期脑血肿液中 IL - 6和 TNFα含量升高 ;脑内炎性细胞因子可能参与血肿周围水肿的形成     

不同剂量纳洛酮对脑出血患者神经功能的保护作用

目的：探讨不同剂量纳洛酮对脑出血患者神经功能的保护作用。方法脑出血患者60例，按照完全抽样法1：1分成2组，对照组予纳洛酮1.2 mg／d治疗，研究组予纳洛酮4.0 mg／d治疗，分析2组临床症状与疗效性指标情况。结果2组治疗7 d时B‐内啡肽、亮氨酸脑啡肽与强啡肽 A1‐13均上升，组间比较差异有统计学意义（ P＜0.05）；研究组血肿体积（18.76±3.07）mL ，治疗14 d时的NDS评分（8.64±5.78）分均比对照组（24.09±5.16）mL、（13.75±5.74）分低，差异有统计学意义（P＜0.01）；研究组治疗后的GCS评分比治疗前与对照组高，治疗14 d时的阿片肽含量均比治疗前与对照组低，差异有统计学意义（ P＜0.05）。结论高剂量纳洛酮治疗脑出血，可减少脑部血肿体积，降低体内阿片肽含量，具有较好的神经功能保护作用。     

超早期运用重组活化凝血因子Ⅶ减少高血压脑出血继续出血研究

目的：分析超早期运用重组活化凝血因子Ⅶ减少高血压脑出血继续出血的临床效果。方法将118例高血压脑出血患者随机分为研究组和对照组,每组59例。对照组患者于发病后3 h内给予止血敏1.0 g静脉注射;研究组于发病后3 h内给予重组活化凝血因子Ⅶ40μg／kg静脉注射。比较2组患者用药24 h后颅内血肿体积变化情况、用药72 h后颅内总病变体积变化、NIHSS评分和Barthel指数。结果治疗前2组血肿体积比较差异无统计学意义（t＝1.50,P＞0.05）,治疗24 h后,对照组和研究组患者的血肿体积分别为（30.12±9.21）mL 和（21.91±9.54）mL ,差异有统计学意义（t＝4.70,P＜0.01）;治疗72 h后血肿＋水肿体积分别为（35.3±10.27）mL和（25.94±10.28）mL ,差异有统计学意义（t＝4.89,P＜0.01）。治疗前2组NIHSS评分和Barthel指数比较差异无统计学意义（P＞0.05）,治疗后24 h、72 h、15 d、90 d差异均有统计学意义（P＜0.01）。结论超早期运用重组活化凝血因子Ⅶ减少高血压脑出血继续出血临床效果显著,可有效降低继续出血量以减少血肿体积增加和脑神经损伤,增加患者生活能力。     

局部激素缓释片应用对脑内血肿清除后脑水肿的影响

目的研究局部应用地塞米松缓释片对兔脑内血肿清除术后脑水肿的影响。方法32只兔子随机分为A（对照组）和B（治疗组）两组并应用自体血注射法建立脑内血肿模型。A组行常规血肿清除术；B组于血肿清除术后，在血肿残腔内置入地塞米松缓释片。检测两组兔脑组织含水量和血清髓鞘碱性蛋白（MBP）水平并比较。结果A、B两组患侧大脑半球含水量分别为（83．61±0．62）％和（81．53±0．59）％，B组显著低于A组（P〈0．05）。A、B两组血清MBP分别为（6．18±2．13）μg／L和（3．35±1．29）μg／L，均高于正常对照值（1．78±0．76）μg／L，且A组显著高于B组（P〈0．05）。结论脑内血肿清除术后脑组织含水量及血清MBP增高，局部应用地塞米松缓释片后显著降低，提示该方法是预防和治疗脑内血肿清除术后脑水肿的有效方法。     

高血压脑出血患者血清和颅内血肿液中IL-1β、IL-6、TNF—α的含量研究

目的通过测定高血压脑出血患者静脉血清及颅内血肿液中白细胞介素-1β（IL-1β）、白细胞介素．6（IL-6）、肿瘤坏死因子-α（TNF—α）水平,探讨这些炎症因子与脑出血病灶及外周血之间的关系。方法在高血压脑出血后24h,72h,7d和14d取80例高血压脑出血患者静脉血清及血肿液检测IL-1β、IL-6、TNF-α的含量（实验组）,并与30例正常体检的患者（对照组）对比。结果高血压脑出血患者血肿液IL-1β、IL-6、TNF-α含量显著高于对照组人群静脉血,并且显著高于实验组患者自身静脉血。实验组患者静脉血清中IL-1β、IL-6、TNF-α含量显著高于对照组人群静脉血清,且病情越重几种炎症因子水平越高。脑出血不同时期静脉血清IL-1β、IL-6、TNF—α．含量比较,在72h最高,此后呈下降趋势。结论高血压脑出血患者IL-1β、IL-6、TNF-α参与了脑出血的炎症反应,是脑出血后脑组织损伤的重要机制之一。     

高血压性脑出血患者不同体液TNF-α水平动态变化及意义

目的探讨高血压性脑出血患者血清、脑脊液、血肿液中TNF-α水平及在不同治疗方式下的动态变化。方法采用放射免疫法检测67例高血压性脑出血患者(分为微创术组和内科组)出血后24h及治疗后72h、7d、14d血清、脑脊液、血肿液中TNF-α含量,并评定以上各时段NIHSS评分。结果高血压性脑出血患者血清TNF-α水平明显升高,经钻颅微创颅内血肿碎吸术治疗72h血清TNF-α水平明显高于内科治疗组(P0.05),微创术组在术后30min及72h脑脊液TNF-α水平均明显高于内科治疗组(P0.01),7d后2组差异无统计学意义(P0.05)。各时段血清TNF-α水平均与NIHSS评分呈正相关(P0.01)。不同时段三种体液中TNF-α水平比较显示,72h三种体液中均达到高峰,随后逐渐降低,脑脊液及血肿液浓度均高于血清。结论高血压性脑出血患者血清TNF-α水平升高,并随病程进展动态变化,与症状严重程度相关,该因子有可能参与脑出血后神经功能损伤的一系列病理生理过程。     

骨桥蛋白与高血压性脑出血脑组织水肿程度和神经功能损伤及临床预后的相关性分析

目的 观察高血压性脑出血（HICH）患者骨桥蛋白（OPN）的表达及其与脑组织水肿程 度、神经功能损伤及临床预后之间的关系。方法 收集临沂市人民医院神经内科监护室自 2017 年 4 月 至 2018 年 11 月收治的 HICH 患者 17 例为观察组，通过立体定向软通道颅内血肿清除术取其血肿液， 并同时抽取患者外周血。测量观察组脑组织出血量、水肿量，并评估术前格拉斯哥昏迷量表（GCS）评 分、美国国立卫生研究院卒中量表（NIHSS）评分，术后 3 个月改良 Rankin 量表（mRS）评分。收集临沂 市人民医院 14 例健康体检者为对照组，取其空腹外周血。利用酶联免疫吸附剂测定（ELISA）法检测 观察组血肿液、外周血和健康对照组外周血 OPN 水平，分析 OPN 表达水平与患者脑水肿程度、神经功 能损伤及临床预后之间的关系。结果 观察组患者血肿液中 OPN 水平高于患者外周血［（2 653.48± 1 460.64）μg/L 比（1 313.00±950.89）μg/L］，差异有统计学意义（t=4.752，P＜ 0.001）。观察组患者外 周血 OPN 水平与对照组外周血［（1 313.00±950.89）μg/L 比（923.44±284.73）μg/L］差异无统计学意 义（t=1.475，P=0.151）。轻中度、重度神经功能障碍组血肿液 OPN 水平分别为（1 708.87±1 227.78）、 （3 716.16±846.08）μg/L，差异有统计学意义（t=3.872，P=0.002）。轻、中、重度意识障碍组血肿液OPN水平 差异有统计学意义［（1 378.30±626.26）μg/L 比（1 798.04±1 518.76）μg/L 比（3 507.14±1 000.53）μg/L； F=4.987，P=0.023］。少量、大量脑水肿组血肿液 OPN 水平差异有统计学意义［（1 418.08±851.40）μg/L 比（3 751.61±865.90）μg/L，t=5.590，P＜ 0.001］。预后良好、预后不良组血肿液 OPN 水平差异有统计学 意义［（2 006.46±994.69）μg/L 比（3 882.90±482.28）μg/L；t=4.232，P=0.001］。血肿液 OPN 浓度与水肿 量（r=0.616，P=0.008）、发病时 GCS 评分（r=0.491，P=0.045）、发病时 NIHSS 评分（r=0.491，P=0.046）、术后 3 个月 mRS 评分（r=0.581，P=0.029）均呈正相关。结论 OPN 与 HICH 患者病情严重程度及预后具有相 关性，血肿液中 OPN 水平越高，病情越重，预后越差。     

脑出血患者血浆及脑脊液内皮素—1含量对照研究

本文对照研究了脑出血患者血浆及脑脊液（ＣＳＦ）内皮素－１（ＥＴ－１）含量改变及其临床意义。发现脑出血患者血浆与ＣＳＦ、ＥＴ－１含量均增高；单纯脑血肿者以血浆含量增高为主；脑实质出血伴有脑室系统或蛛网膜下腔出血（ＳＡＨ）者血浆及ＣＳＦ含量均显著升高；小量出血与中大量出血比较血浆含量无显著性，而大量出血者ＣＳＦ、ＥＴ－１含量增高。提示脑出血者血浆ＥＴ－１增高可能与机体应激有关，而ＣＳＦ、ＥＴ－１升高可     

脑出血患者血浆及脑脊液内皮素－1含量对照研究

本文对照研究了脑出血患者血浆及脑脊液（ＣＳＦ）内皮素－１（ＥＴ－１）含量改变及其临床意义。发现脑出血患者血浆与ＣＳＦ、ＥＴ－１含量均增高；单纯脑血肿者以血浆含量增高为主；脑实质出血伴有脑室系统或蛛网膜下腔出血（ＳＡＨ）者血浆及ＣＳＦ含量均显著升高；小量出血与中大量出血比较血浆含量无显著性，而大量出血者ＣＳＦ、ＥＴ－１含量增高。提示脑出血者血浆ＥＴ－１增高可能与机体应激有关，而ＣＳＦ、ＥＴ－１升高可能与血脑屏障（ＢＢＢ）被破坏及损害或刺激室周组织、下丘脑、脉络丛脑膜，引起分泌释放增加有关。ＣＳＦ、ＥＴ－１增高者应警惕迟发性脑血管痉挛。     

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.     

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.     

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.     

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.