阿托伐他汀对老年缺血性脑卒中患者氧化应激及脂质过氧化的影响

目的观察阿托伐他汀对老年缺血性脑卒中(CIS)的治疗效果及对患者体内氧化应激及脂质过氧化状态的影响。方法随机选取河南宏力医院2012-01—2015-02经颅脑CT与MRI检查证实为缺血性脑卒中的57例患者进行研究,患者年龄均60岁。按住院床位单双号分为常规组(n=28)与治疗组(n=29),所有患者入院后第一时间测定血浆中8-异前列腺素(8-iso-PGF2α)与氧化低密度脂蛋白(ox-LDL)水平。常规组行神经内科常规治疗,但不予以他汀类药物,治疗组常规内科治疗的基础上采取阿托伐他汀药物口服,观察2组患者治疗后恢复效果及氧化应激和脂质过氧化水平。结果治疗前2组NIHSS评分,ADL评分差异无统计学意义(P0.05),治疗后2组NIHSS评分,ADL评分差异有统计学意义(P0.05);常规组8-iso-PGF2α与ox-LDL水平较治疗组有更明显增长,差异有统计学意义(P0.05)。结论老年CIS患者在常规内科治疗的基础上使用阿托伐他汀药物可有效控制8-iso-PGF2α与ox-LDL水平,改善患者氧化应激及脂质过氧化状态,促进神经功能的恢复,对预后有积极作用。     

阿托伐他汀对老年急性脑梗死患者治疗效果及影响

目的探究阿托伐他汀对老年急性脑梗死患者的治疗效果及影响。方法选取老年急性脑梗死(发病48h内)患者68例,男46例,女22例,平均年龄(61.0±7.5)岁。随机数字法均分为阿托伐他汀治疗组与对照组,对照组予硝苯地平缓释片、阿司匹林肠溶胶囊、甘露醇行降颅内压、抗凝治疗;治疗组在对照组基础上给予阿托伐他汀,观察2组治疗后的血清指标。结果治疗12周末,2组患者血浆hs-CRP及血清MMP-9水平较本组治疗前均显著下降,且组间比较,阿托伐他汀组比对照组下降更显著(P0.05);阿托伐他汀组较治疗前TC、TG、LDL-C、IMT有所下降,HDL-C升高(P0.05),与对照组治疗12周末组间比较,显著低于对照组,HDL-C显著高于对照组,P0.05;NIHSS评分阿托伐他汀组重型(17.11±3.01)、中型(7.13±2.48)、轻型(2.66±0.99)显著低于对照组,MBI评分(96.31±7.53)显著高于对照组(87.22±6.21);2组有不同程度的不良反应,如恶心、头晕、便秘等(对照组分别为1、1、3例,阿托伐他汀组分别为1、2、1例,P0.05),患者未停止给药或特殊治疗,不良症状耐受。结论在老年脑梗死患者治疗中,阿托伐他汀疗效明确、能降低血脂、抑制动脉粥样硬化、减轻机体炎症反应,改善血管内皮功能及改善患者脑梗死早期预后,能有效减轻神经功能损伤、且安全不良反应小,作为治疗老年急性脑梗死的核心药物值得基层医院、门诊推广应用。     

阿托伐他汀对脑梗死患者血脂、颈动脉内-中膜厚度及复发率的影响

目的 研究阿托伐他汀对脑梗死患者的血脂、颈动脉内-中膜厚度(IMT)及复发率的影响.方法 59例合并有高脂血症和颈动脉粥样硬化的脑梗死患者随机分为阿托伐他汀组(29例)和对照组(30例).两组患者均给予脑梗死常规治疗;阿托伐他汀组患者加用阿托伐他汀20 mg/d,连用12个月.在治疗前及治疗后3、6、12个月时,检测患者的血脂,用彩色多普勒超声仪检测颈动脉内-中膜厚度(IMT).统计治疗后12个月时脑梗死复发的例数.结果 阿托伐他汀组治疗后各时间点的血胆固醇(TC)、低密度脂蛋白(LDL)水平显著低于治疗前及对照组(均P＜0.01);治疗后12个月时高密度脂蛋白(HDL)水平显著高于治疗前及对照组(均P ＜0.05).阿托伐他汀组治疗后6个月、12个月时颈动脉IMT显著低于治疗前及对照组(P ＜0.05 ～0.01);对照组治疗后12个月时则明显高于治疗前(P＜0.05).治疗12个月后,阿托伐他汀组无脑梗死复发,对照组脑梗死复发3例(10％).结论 阿托伐他汀能显著降低脑梗死患者的血TC、LDL水平,长期治疗可降低颈动脉IMT和脑梗死的复发率.     

阿托伐他汀治疗急性脑梗死的疗效及安全性分析

目的探讨阿托伐他汀治疗急性脑梗死患者的效果及安全性。方法将100例急性脑梗死患者随机分成观察组与对照组,每组50例,对照组给予常规治疗与对症治疗,治疗组在对照组基础上加服阿托伐他汀,比较2组患者治疗前后的氧化应激指标水平、颈动脉斑块的改变及不良反应状况。结果观察组治疗后的氧化低密度脂蛋白(oxLDL)、丙二醛(MDA)等指标水平显著降低,超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)等指标水平显著升高,且观察组治疗后的各氧化应激指标(oxLDL、MDA、SOD、GSH-Px)水平与对照组相比,差异均有统计学意义(P0.05);观察组治疗后的斑块Crouse积分、颈动脉内中膜厚度(IMT)等均显著下降,且Crouse积分、IMT均显著低于对照组,差异有统计学意义(P0.05);2组不良反应发生率对比,差异无统计学意义(P0.05)。结论采用阿托伐他汀治疗急性脑梗死患者,可有效减轻氧化应激损伤、缓解颈动脉粥样硬化,安全性较高,具有较高的应用价值。     

羟乙基淀粉联合阿托伐他汀改善分水岭脑梗死患者神经功能缺损程度的作用

目的：探讨羟乙基淀粉与阿托伐他汀在改善分水岭脑梗死患者神经功能缺损程度中的作用。方法100例分水岭脑梗死患者随机分为2组,对照组单纯口服阿托伐他汀治疗,观察组联合应用阿托伐他汀和羟乙基淀粉。比较2组神经功能缺损改善程度和临床疗效。结果治疗后观察组NIHSS评分明显低于对照组（P＜0.05）,ADL评分明显高于对照组（P＜0.05）;观察组痊愈率30％,总有效率96％,均明显高于对照组的20％、80％（ P＜0.05）;观察组肺部感染、上消化道出血、脑血管病后抑郁症等不良反应发生率均明显低于对照组（ P＜0.05）。结论羟乙基淀粉联合阿托伐他汀能够显著改善分水岭脑梗死患者的神经功能缺损程度。     

盐酸小檗碱联合阿托伐他汀治疗急性脑梗死的疗效及对颈动脉粥样硬化斑块的影响

目的观察盐酸小檗碱联合阿托伐他汀治疗急性脑梗死(ACI)的疗效及对颈动脉粥样硬化斑块的影响。方法将84例ACI患者随机分为2组,对照组(n=42)加用阿托伐他汀片,观察组加用阿托伐他汀片+盐酸小檗碱片,比较2组患者治疗前及6个月后的临床疗效以及颈动脉粥样硬化斑块的影像学结果。结果治疗6个月后,2组TG、TC、LDL-C均较治疗前显著降低(P0.05),且观察组的降低幅度大于对照组(P0.05);治疗6个月后,观察组患者的IMT值、Crouse积分、不稳定性斑块数目均较治疗前显著降低(P0.05)。结论盐酸小檗碱联合阿托伐他汀能够有效降低ACI患者的血脂水平和Crouse积分,具有较好的抗动脉粥样硬化作用。     

瑞舒伐他汀与阿托伐他汀对急性脑梗死患者血脂、血清超敏C反应蛋白及颈动脉粥样硬化斑块作用的比较

目的比较瑞舒伐他汀与阿托伐他汀对急性脑梗死患者血脂、超敏C反应蛋白(hs-CRP)及颈动脉粥样硬化斑块的影响。方法在标准缺血性脑卒中治疗的基础上,瑞舒伐他汀组加用瑞舒伐他汀10mg/d,阿托伐他汀组加用阿托伐他汀片20 mg/d,治疗6个月。于治疗前及治疗后6个月,检测患者血脂、hsCRP水平,颈动脉超声检查颈动脉粥样硬化斑块情况。结果与治疗前比较,瑞舒伐他汀组与阿托伐他汀组6个月时总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)和hs-CRP水平均显著降低(均P0.05)。6个月时,瑞舒伐他汀组TC、TG、LDL-C及hs-CRP水平显著低于阿托伐他汀组及对照组(均P0.05)。3组间治疗前内-中膜厚度(IMT)差异无统计学意义;与治疗前及对照组比较,瑞舒伐他汀组与阿托伐他汀组6个月时IMT及低回声斑块比率显著降低,高回声斑块率显著增高(均P0.05)。瑞舒伐他汀组、阿托伐他汀组及对照组患者第6个月的NIHSS评分及mRS评分均显著低于治疗前(均P0.05)。治疗前及治疗后6个月时,3组间NIHSS评分及mRS评分差异无统计学意义。结论瑞舒伐他汀与阿托伐他汀能显著降低急性脑梗死患者血脂及血清hs-CRP水平,抑制动脉粥样硬化斑块的形成。瑞舒伐他汀的降脂及抗炎作用比阿托伐他汀更强。     

阿托伐他汀辅助治疗老年单纯收缩期高血压疗效分析

目的观察分析阿托伐他汀辅助治疗老年单纯收缩期高血压的临床疗效。方法选取我院门诊110例治疗原发性老年高血压患者,随机分为对照组和观察组。对照组给予口服血管紧张素转化酶抑制剂（ACEI）及钙通道阻滞剂等降压药物治疗;观察组在上述治疗基础上加用阿托伐他汀治疗,分别于治疗第4、8、12周检测患者收缩压（SBP）、舒张压（DBP）、脉压（PP）。结果治疗第4、8周后,2组患者SBP、DBP及PP无显著差异（P〉0.05）;对照组第12周SBP与观察组比较（t=16.227,P=0.0001）,对照组第12周PP与观察组比较（t=13.818,P=0.0001）,差异均有统计学意义（P〈0.05）。结论阿托伐他汀联合降压药物可明显降低患者收缩压和脉压,改善患者动脉血管顺应性,治疗剂量下患者耐受性良好,不良反应轻微。     

阿托伐他汀联合氯吡格雷对脑梗死患者hs-CRP MMP-9 TNF-α IMT及血脂的影响

目的探讨阿托伐他汀联合氯吡格雷治疗对脑梗死患者hs-CRP、MMP-9、TNF-α、IMT及血脂的影响。方法选取来我院治疗的脑梗死患者90例为研究对象,随机分为观察组和对照组,每组45例。对照组给予氯吡格雷治疗,观察组给予阿托伐他汀联合氯吡格雷治疗。测定并比较2组患者治疗前后血清hs-CRP、MMP-9和TNF-α水平、内膜中层厚度(IMT)及血脂水平。结果治疗后观察组血清hs-CRP、MMP-9和TNF-α水平明显低于对照组,差异有统计学意义(P0.05);2组患者颈动脉IMT变薄,与治疗前比较差异均有统计学意义(P0.05),且观察组治疗后IMT较对照组减少(P0.05);治疗后2组患者血清血脂水平均明显下降,组间比较差异无统计学意义(P0.05)。结论阿托伐他汀联合氯吡格雷治疗脑梗死患者能更有效地降低血hs-CRP和MMP-9水平,使IMT变薄,更有利于抑制炎症从而降低卒中发病率,值得临床推广。     

不同剂量阿托伐他汀联合氯吡格雷治疗短暂性脑缺血发作的疗效及对预后的影响

目的探讨不同剂量阿托伐他汀联合氯吡格雷治疗短暂性脑缺血发作(TIA)的疗效及对预后的影响。方法66例TIA患者随机分为2组,对照组予阿托伐他汀(20mg/d)联合氯吡格雷治疗,观察组予高剂量阿托伐他汀(40mg/d)联合氯吡格雷治疗,比较2组近期疗效及随访12个月TIA复发次数、脑梗死发生率。结果 2组总有效率比较差异无统计学意义(P0.05),但观察组基本痊愈率(75.76%)显著高于对照组(51.52%),差异有统计学意义(P0.05);随访12个月观察组TIA复发次数明显少于对照组,脑梗死发生率也低于对照组,差异均有统计学意义(P0.05)。结论高剂量阿托伐他汀(40mg/d)联合氯吡格雷治疗TIA可快速有效控制临床症状,减少复发并阻止TIA的进一步发展。     

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.     

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.     

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.     

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.     

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.     

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.