强化降脂治疗冠心病合并脑梗死临床观察

目的观察强化降脂在冠心病合并脑梗死治疗中的作用。方法选取146例冠心病合并脑梗死患者为研究对象,随机分为强化降脂组与常规降脂组,每组73例。强化降脂组给予大剂量阿托伐他汀治疗,常规降脂组给予常规剂量阿托伐他汀治疗,比较2组血脂水平、炎症因子与不良反应。结果强化降脂组治疗后总胆固醇(TC)、低密度脂蛋白水平(LDL-C)、超敏C反应蛋白(hs-CRP)显著低于常规降脂组(P0.05)。结论强化降脂治疗冠心病合并脑梗死可以降低血脂水平,抑制炎症反应,减少心脑血管事件的发生。     

瑞舒伐他汀与辛伐他汀治疗缺血性脑卒中的疗效比较

目的探讨瑞舒伐他汀与辛伐他汀治疗缺血性脑卒中的疗效。方法选取我院缺血性脑卒中患者90例,随机分为2组,观察组45例在基础治疗基础上加用瑞舒伐他汀,对照组45例在基础治疗基础上加用辛伐他汀,比较治疗前与治疗3个月后患者空腹静脉血中总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)及超敏C反应蛋白(hs-CRP)的变化。观察2组不良反应。结果治疗后2组TC、TG、LDL-C、hs-CRP水平均显著低于治疗前,HDL-C水平显著高于治疗前,且瑞舒伐他汀组变化幅度更大,差异均有统计学意义(P<0.05)。瑞舒伐他汀组与辛伐他汀组的缺血性脑卒中复发率分别为11.11%(5/45)和24.44%(11/45),2组比较差异有统计学意义(P<0.05)。观察组不良反应较轻微,与对照组相比,差异有统计学意义(P<0.05)。结论瑞舒伐他汀与辛伐他汀对于缺血性脑卒中患者均有很好的降脂及抗炎作用,且不良反应情况类似,但瑞舒伐他汀效果更为显著且复发率更低。     

SLCO1B1 521T>C基因多态性对瑞舒伐他汀钙降脂疗效的影响

目的观察SLCO1B1 521TC基因多态性对瑞舒伐他汀钙降脂疗效的影响。方法纳入2015年1月-2015年12月期间我院神经内科高脂血症患者,均口服瑞舒伐他汀钙片10 mg,一次/日,睡前服用。应用ARMS-PCR方法探索中国人群中SLCO1B1 521TC的基因型分布频率,并分别检测用药前与用药后1 w、6 w的血总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)及高密度脂蛋白胆固醇(HDL-C),并计算其变化率。结果瑞舒伐他汀治疗1 w后,各组TC、TG、LDL-C、HDL-C变化率差异均无统计学意义(P0.05)。用药6 w后,TC组和CC组较TT组能显著降低TC、LDL-C及升高HDL-C水平,有统计学意义(P0.01),但TC组和CC组间差异无统计学意义(P0.05)。各组间TG变化率差异无统计学意义(P0.05)。结论 SLCO1B1 521TC基因变异可增强瑞舒伐他汀钙降脂疗效。     

强化降脂对缺血性脑卒中患者血脂及颈动脉粥样硬化的影响

目的 观察强化降脂治疗对缺血性卒中患者血脂及颈动脉粥样硬化的影响.方法 随机将102例有血脂异常及颈动脉粥样硬化的缺血性卒中患者分为阿托伐他汀常规治疗组(20mg/d)与强化降脂治疗组(40mg/d),每组51例,分别于用药前、用药后6m检测血脂,颈动脉超声测定颈动脉内膜中层厚度(CIMT)变化.结果 治疗后6m,两组总胆固醇(TC)、低密度脂蛋白(LDL-C)、甘油三脂(TG)水平均降低,高密度脂蛋白胆固醇(HDL-C)均有升高,强化降脂组较常规降脂组血脂变化更明显(P＜0.05或P＜0.01),强化降脂组CIMT、斑块面积较常规治疗组降低更明显(P＜0.05),强化降脂组缺血性脑血管病复发率较常规组明显降低(P＜0.05),两组不良反应发生率比较无统计学意义.结论 强化降脂治疗能有效改善缺血性卒中患者血脂水平,有效延缓和逆转颈动脉粥样硬化斑块,减少缺血性脑血管的复发率,且安全性良好.     

瑞舒伐他汀对缺血性脑卒中患者血清TCTGLDL-C及HDL-C水平变化的影响

目的探讨瑞舒伐他汀对缺血性脑卒中患者血清三酰甘油(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)水平变化的影响。方法选取平煤神马医疗集团总医院收治的68例缺血性脑卒中患者,依据建档顺序分为2组各34例。对照组采用常规治疗措施,研究组在常规治疗基础上加用瑞舒伐他汀,连续服用6个月。统计对比2组入院时及疗程结束后血清TG、TC、HDL-C、LDL-C水平及神经功能缺损评分(NIHSS)、日常生活活动能力评分(BI)、血清炎症因子[白细胞介素-6(IL-6)、IL-10、IL-17]水平变化情况,并统计对比2组不良反应发生率。结果治疗前2组TG、TC、HDL-C、LDL-C水平比较,差异无统计学意义(P0.05),治疗后研究组TG、TC、LDL-C水平低于对照组,HDL-C水平高于对照组,差异有统计学意义(P0.05);治疗前2组NIHSS评分及BI评分比较,差异无统计学意义(P0.05),治疗后研究组NIHSS评分低于对照组,BI评分高于对照组,差异有统计学意义(P0.05);治疗前2组IL-6、IL-10、IL-17水平比较,差异无统计学意义(P0.05),治疗后研究组IL-6、IL-17水平低于对照组,IL-10水平高于对照组,差异有统计学意义(P0.05);研究组不良反应发生率(17.64%)与对照组(14.70%)比较,差异无统计学意义(P0.05)。结论采用瑞舒伐他汀治疗缺血性脑卒中效果显著,可有效改善患者血脂及血清炎症因子水平,提高神经功能及日常生活能力,且安全性较高。     

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。     

阿托伐他汀联合苯磺酸氨氯地平治疗冠心病合并脑梗死的疗效及对血脂水平的影响

目的分析阿托伐他汀及苯磺酸氨氯地平治疗冠心病合并脑梗死患者的疗效及对血脂指标的影响。方法选择我院2014-03—2016-03冠心病合并脑梗死患者96例,通过随机数字表法分为研究组和对照组各48例。对照组给予苯磺酸氨氯地平片治疗,研究组给予阿托伐他汀及苯磺酸氨氯地平片治疗。观察2组临床疗效、不良反应发生情况,并比较治疗前后2组血脂相关指标[总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)]水平变化情况。结果研究组总有效率(93.75%)明显高于对照组(77.08%),差异显著(P0.05);治疗前研究组HDL-C、LDL-C、TG、TC水平与对照组比较差异无统计学意义(P0.05),治疗后研究组各指标水平优于对照组,差异有统计学意义(P0.05);2组不良反应发生率比较差异无统计学意义(P0.05)。结论给予冠心病合并脑梗死患者阿托伐他汀及苯磺酸氨氯地平片可取得良好效果,能改善患者血脂水平,提高治疗效果,且不会增加不良反应发生率,具有安全性。     

阿托伐他汀降脂治疗对脑微出血的影响

目的探讨阿托伐他汀降脂治疗对脑微出血的影响。方法 48例大动脉动脉粥样硬化性脑梗死合并脑微出血患者根据其血脂水平等分为强化降脂组(20例)、标准降脂组(14例)和非降脂组(14例);入组者在脑血管病常规治疗的基础上,强化及标准降脂治疗组分别给予阿托伐他汀平均(18.6±9.9)mg/d或(7.7±3.0)mg/d 3个月。治疗前后分别行磁敏感加权成像(SWI)检查脑微出血灶数以及血清总胆固醇(TC)、低密度脂蛋白(LDL)水平检测。结果强化及标准降脂组治疗后血清TC、LDL水平较治疗前显著下降(均P<0.05),非降脂组治疗前后血脂水平无明显变化;各组间治疗前后脑微出血灶数目差异无统计学意义。结论阿托伐他汀短期降脂治疗对脑微出血无明显影响。     

氯吡格雷联合氟伐他汀治疗脑梗死的疗效观察

目的观察氯吡格雷联合氟伐他汀治疗脑梗死的疗效及对患者生存质量的影响。方法选取2016-01—12在我院治疗的脑梗死患者96例为研究对象,采用随机数表法分为观察组(48例)与对照组(48例)。对照组实施常规治疗措施,观察组给予氯吡格雷联合氟伐他汀治疗。观察2组临床疗效、治疗前后生存质量、血脂水平与不良反应等。结果观察组总有效率显著高于对照组,差异有统计学意义(P0.05);治疗后观察组TC、TG、LDL-C均低于对照组,HDL-C与生存质量评分高于对照组,差异有统计学意义(P0.05);2组不良反应发生率比较,差异无统计学意义(P0.05)。结论氯吡格雷联合氟伐他汀治疗可改善脑梗死患者的血脂水平,显著改善其生存质量及预后。     

氟伐他汀对脑梗死患者颈动脉粥样斑块干预治疗的临床观察

目的观察氟伐他汀对脑梗死患者血脂、炎性因子水平及颈动脉粥样硬化的影响。方法选择90例脑梗死患者,将患者随机分为3组,每组30人:A组(对照组)采用脑梗死常规治疗,氟伐他汀治疗组B组(40mg组)和C组(80mg组),B、C组在常规治疗基础上每晚分别口服氟伐他汀40mg、80mg。所有患者均于治疗前及治疗后6个月测定血脂、超敏C反应蛋白(hs-CRP)、基质金属蛋白酶-9(MMP-9)水平及颈动脉粥样硬化情况。结果经过治疗6个月后,A组TC、TG、LDL-C、HDL-C、hs-CRP、MMP-9水平及颈动脉斑块积分、不稳定斑块数量、IMT较治疗前无明显改变(P>0.05);B、C两组TC、TG、LDL-C、hs-CRP、MMP-9显著下降,HDL-C升高,与A组比较差异有统计学意义(P<0.05),其中C组TC、TG、LDL-C、hs-CRP、MMP-9水平下降更明显(P<0.05);C组治疗后颈动脉斑块积分、不稳定斑块数量、IMTP明显减少,与A组比较差异有统计学意义(P<0.05),而B组下降不明显(P>0.05);三组NDS较治疗前均明显降低(P<0.05),三组之间差异有统计学意义(P<0.05)。结论氟伐他汀能有效降低脑梗死患者血脂、炎性因子水平,改善颈动脉粥样硬化,以80mg剂量效果显著。     

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.     

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.     

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.