三种不同病因缺血性脑卒中急性期血压与预后的关系

目的 探讨三种不同病因类型的缺血性脑卒中急性期血压与预后的关系.方法 以温州脑卒中登记库为基础,前瞻性连续登记2007年4月至2008年4月温州医学院附属第一医院从发病到入院时间小于48 h并被诊断为脑梗死的患者.采用Logistic多因素逐步回归法分析不同病因型脑梗死患者影响预后的因素.结果 各病因型入院血压和急性期平均血压与预后均呈U型关系.动脉粥样硬化型、心源性栓塞型和其他病因型入院时血压在150/95 mm Hg(1 mm Hg=0.133 kPa)左右,7 d内平均血压140/90 mm Hg时预后最佳;小动脉病变型以入院时血压在130/95 mm Hg左右,7 d内平均血压140/90 mm Hg时预后最佳.在动脉粥样硬化型缺血性脑卒中患者中,入院24 h内收缩压下降幅度大于20 mm Hg使3个月的死亡和残疾风险增加4.44倍(OR 4.44,95%CI 1.70～11.59,P=0.002);入院24 h内舒张压下降幅度大于10 mm Hg使3个月的死亡和残疾风险增加3.70倍(OR 3.70,95%CI 1.54～8.90,P=0.00).心源性脑栓塞患者中,入院24 h内收缩压下降幅度大于20 mm Hg(OR 7.98,95%CI 1.34～47.66,P=0.026)和舒张压下降幅度大于10 mm Hg(OR6.68,95%CI 1.55～28.79,P=0.01)均为3个月死亡和残疾的独立危险因素.结论 入院时各亚型组的血压与3个月病死和残疾率均呈U型关系,血压过高或过低患者预后均较差.对于动脉粥样硬化型患者和心源性栓塞患者,入院24 h内血压下降幅度过大为其3个月预后不良的独立危险因素.     

重症缺血性脑卒中预后相关影响因素分析

目的探讨影响重症缺血性脑卒中(sIS)短期预后的相关因素。方法回顾性分析143例缺血性脑卒中(IS)住院患者的一般资料和实验室检查,包括既往史、血常规、血生化、凝血象等指标,头颅CT或MRI影像资料,发病后的并发症。根据美国国立卫生研究院卒中量表(NIHSS)评分变化进行病情严重程度分类及预后判断。结果 143例IS患者中sIS者82例(57.3%),轻症缺血性脑卒中(mIS)61例(42.7%)。82例sIS患者中,预后不良的发生率为73.2%(60/82)。sIS预后改善与预后不良组间入院收缩压、低密度脂蛋白(LDL-C)、随机血糖(Glu)比较差异有统计学意义(P<0.05);多因素Logistic回归分析显示,LDL-C水平升高是sIS早期不良预后的独立危险因素(OR=1.68,95%CI:1.05～2.69),入院时收缩压相对升高对sIS的预后具有保护作用(OR=0.97,95%CI:0.05～1.00)。mIS 30d预后不良组与sIS 30d预后不良组间房颤、卒中相关肺炎(SAP)、血白细胞数升高比较有统计学差异(P<0.05);多因素Logistic回归分析显示,房颤(OR=5.04,95%CI:1.31～9.63)、SAP(OR=3.23,95%CI:1.12～9.36)是IS早期不良预后的独立危险因素。结论房颤、LDL-C水平升高、SAP是IS早期预后不良的独立危险因素。     

入院时中性粒细胞与淋巴细胞比值和血糖水平对急性脑出血患者短期预后不良的预测价值

目的分析急性脑出血患者短期预后不良的相关危险因素,并探讨入院时中性粒细胞与淋巴细胞比值(neutrophil-to-lymphocyte ratio,NLR)和入院即刻血糖水平(admission blood glucose,ABG)对短期预后不良的预测价值。方法收集2017-01-2018-05期间作者医院收治的急性脑出血患者226例,根据3个月时改良Rankin评分量表(modified Rankin scale,mRS)评分分为预后良好(mRS≤2分)组124例,预后不良(mRS2分)102例,单因素分析两组患者入院时的临床、影像学及实验室资料,采用二分类Logistic回归分析探讨影响急性脑出血患者短期预后不良的危险因素,采用受试者工作特征(receiver operating characteristic,ROC)曲线评价NLR和ABG对短期预后不良的预测价值。结果 (1)与预后良好组相比,预后不良组患者糖尿病病史、饮酒史比例以及年龄、美国国立卫生研究院卒中量表(National Institute of Health stroke scale,NIHSS)评分均升高,血肿体积大,出血破入脑室比例高,白细胞计数(ABC)、中性粒细胞计数(ANC)、NLR及ABG升高,淋巴细胞计数(ALC)低(均P0.05)。(2)二分类Logistic回归分析显示患者年龄(OR=1.051,95%CI:1.013～1.090,P0.01)、血肿体积(OR=1.055,95%CI:1.003～1.110,P0.05)、NLR(OR=1.389,95%CI:1.124～1.716,P0.01)、ABG(OR=1.308,95%CI:1.074～1.593,P0.05)及NIHSS评分(OR=1.151,95%CI:1.065～1.243,P0.01)升高为急性脑出血患者短期预后不良的独立危险因素。(3)ROC曲线分析表明,NLR和ABG的ROC曲线下面积分别为0.767(95%CI:0.705～0.829,P0.01)、0.678(95%CI:0.609～0.747,P0.05)。结论入院时年龄、血肿体积、NIHSS评分、NLR及ABG升高是急性脑出血患者短期预后不良的独立危险因素,NLR和ABG对急性脑出血患者短期预后不良有一定的预测价值。     

近期单发皮质下梗死患者预后不良危险因素分析

研究背景脑白质高信号为脑小血管病的影像学标志物,常与近期单发皮质下梗死并存。本研究旨在筛查近期单发皮质下梗死患者预后不良相关危险因素。方法纳入2018年6月至2019年12月四川大学华西医院收治的432例近期单发皮质下梗死患者,头部MRI评估脑白质高信号(包括脑室旁白质高信号和脑深部白质高信号)。单因素和多因素Logistic回归分析筛查近期单发皮质下梗死预后不良相关危险因素,分层分析评估该危险因素在不同人群中的稳定性。结果 432例患者根据Fazekas评分分为轻度脑白质高信号组(评分0～3,277例)和重度脑白质高信号组(评分4～6,155例)。Logistic回归分析显示,年龄较大(OR=1.060,95%CI:1.028～1.093;P=0.000)、发病至入院时间较长(OR=1.005,95%CI:1.002～1.008;P=0.001)、入院时NIHSS评分较高(OR=1.109,95%CI:1.047～1.175;P=0.000)、梗死灶直径较大(OR=1.077,95%CI:1.028～1.129;P=0.002)和重度脑白质高信号(OR=2.229,95%CI:1.082～4.591;P=0.030)是近期单发皮质下梗死患者预后不良的危险因素;进一步分层分析显示,在女性(OR=2.460,95%CI:1.120～5.360;P=0.024)、年龄 50岁(OR=1.890,95%CI:1.120～3.180;P=0.017)和高血压(OR=3.150,95%CI:1.230～8.100;P=0.017)患者中,重度脑白质高信号(Fazekas评分4～6)作为近期单发皮质下梗死预后不良的危险因素是稳定的。结论重度脑白质高信号(Fazekas评分为4～6)是近期单发皮质下梗死患者发病3个月时预后不良的危险因素,且在女性、年龄 50岁和高血压人群中具有稳定性。     

血清前清蛋白对急诊初发缺血性脑卒中患者生存状况影响的研究

目的分析血清前清蛋白(PA)对急诊初发缺血性脑卒中患者生存状况的影响。方法选取2013-01-2014-01在我院急诊初发的急性脑梗死患者80例,入院后均按照脑卒中单元的标准指南进行相应的治疗,出院前通过改良Rankin量表(mRS)评分,将患者分为预后良好组(mRS评分0~2分,54例)和预后不良组(mRS评分3~6分,26例)。分别比较2组患者的一般资料、血清PA的差异,采用多因素Logistic回归分析影响患者预后不良的因素。结果 2组比较,患者的起病年龄、冠心病、2型糖尿病、完全前循环梗死(TACI)等级别的患病率明显增高,血清PA水平明显下降,差异有统计学意义(P0.05);多因素Logistic回归分析显示:高龄(OR=1.027,P=0.010)、2型糖尿病(OR=2.384,P=0.004)、冠心病(OR=2.305,P=0.021)和TACI(OR=17.578,P0.001)是急性脑梗死患者预后不良的危险因素,而急性期血清PA水平升高(OR=0.993,P0.001)有利于提高急性脑梗死患者的恢复和生活质量。结论血清PA水平升高对急诊初发缺血性脑卒中患者生存状况有着积极的作用。     

急性缺血性脑卒中静脉溶栓预后的影响因素分析

目的研究急性缺血性脑卒中静脉溶栓预后的影响因素。方法选择96例接受静脉溶栓治疗的急性缺血性脑卒中患者,观察年龄、性别、体质量、高血压史、糖尿病史、吸烟史、溶栓前收缩压、溶栓前血糖、起病-溶栓时间、溶栓前NIHSS评分等指标与预后的关系。结果预后不良组与预后良好组年龄、性别、体质量、高血压史、吸烟史无显著差异(P0.05)。与预后良好组比较,预后不良组糖尿病史比例更高,溶栓前收缩压更高,溶栓前血糖更高,起病-溶栓时间更长,溶栓前NIHSS评分更高(P0.05)。Logistic回归分析示,糖尿病史(OR=4,P=0.032)、溶栓前收缩压(OR=11,P=0.001)、溶栓前血糖(OR=10,P=0.028)、起病-溶栓时间(OR=1.01,P=0.013)、溶栓前NIHSS评分(OR=1.28,P=0.001)与溶栓预后不良显著相关。结论糖尿病史、溶栓前收缩压、溶栓前血糖、起病-溶栓时间、溶栓前NIHSS评分与预后不良密切相关,是预后不良的独立危险因素。     

急性脑梗塞与脑出血相关因素的对比研究

目的:探讨不同危险因素在脑卒中发生的情况及不同危险因素在脑梗死与脑出血间的差异。方法:将收治的卒中患者共408例,其中脑梗死281例,脑出血127例,均预先对各项资料进行编码,输入计算机数据库。所有患者均进行系统的临床和辅助检查,生化指标为集体测定,脑卒中诊断经过MRI或CT确诊。结果:1、高血压、吸烟是脑卒中最重要的危险因素。2、脑出血患者首诊舒张压(P=0．014)、缓解期舒张压(P=0．006)、HDL(P=0．034)、较脑梗塞患者高,其差别有统计学意义;其TC(P=0．047)、吸烟(P=0．007)、心脏病病史(P=0．020)、糖尿病病史(0．000)、卒中家族史(P=0．033)、心脏病家族史(P=0．040)较脑梗塞患者低或少,其差别有统计学差异。3、与脑梗塞相比,吸烟(OR=0. 226,95％CI=0．107—1．623)、糖尿病病史(OR=0．094,95％CI=0．023—2．401)、心脏病病史(OR=0．046,95％CI=0．236-0．905)对脑出血危险较小;高血压病史(OR=1．096,95％CI=0．542-0.895)是脑出血唯一危险因素。结论:高血压、吸烟是脑卒中最重要的危险因素;脑梗塞与脑出血的危险因素并不完全一致。     

非心源性脑梗死患者急性期血压变异与早期神经功能恶化的相关性研究

目的探讨非心源性脑梗死患者急性期24 h血压变异和早期神经功能恶化的关系。方法采用病例对照研究方法连续登记急性非心源性脑梗死患者,收集一般临床资料,连续血压监测并计算24 h血压变异的各参数,按照入院7 d内有无发生脑梗死早期神经功能恶化进行分组比较,建立Logistic回归模型分析24 h血压和血压变异参数与早期神经功能恶化的关系。结果 221例入组患者中59例(26.7%)出现早期神经功能恶化。出现早期神经功能恶化组24 h平均收缩压和收缩压变异系数显著高于未发生组[(145.8±18.2)mm Hg vs.(139.9±20.3)mm Hg;9.0(7.3~11.2)vs.8.4(6.9~10.2)],差异均有统计学意义(P0.05)。多因素校正后,24 h平均收缩压水平和收缩压变异系数增大是发生早期神经功能恶化的独立危险因素(每10 mm Hg 24 h平均收缩压OR=1.285,95%CI(1.059~1.559);收缩压变异系数OR=1.206,95%CI(1.050~1.384))。结论入院后24 h收缩压变异增大是急性非心源性脑梗死7 d内发生早期神经功能恶化的危险因素。     

神经外科重型颅脑创伤急性期血压变异性对患者近期预后的影响研究

目的探讨神经外科重型颅脑创伤(TBI)急性期血压变异性对患者近期预后的影响。方法选取110例重型TBI患者作为研究对象,根据格拉斯哥预后(GOS)评分分为预后良好组(n=53)和预后不良组(n=57),对两组患者术后3d内的血压变异性进行对比分析。结果预后良好组的平均年龄明显低于预后不良组,GCS评分、APACHEⅡ评分均明显高于预后不良组,P0.05。预后良好组入院24h的收缩压标准差、舒张压标准差、收缩压变异系数均显著低于预后不良组,入院72h的收缩压标准差、舒张压标准差、收缩压变异系数、舒张压变异系数均显著低于预后不良组,P0.05。APACHEⅡ评分是患者预后的保护因素,TBI程度、72h SD(SBP)是患者预后的危险因素。结论急性期血压变异性与重型TBI患者的预后密切相关,其影响患者预后的独立危险因素。     

经颅多普勒超声研究我国南方社区人群椎-基底动脉颅内段狭窄的状况

目的 研究我国南方社区健康人群椎-基底动脉颅内段狭窄的患病情况和危险因素.方法 以居委会为单位随机整群抽取社区成年居民.测量身高、体重、腰围、臀围和血压,记录病史资料.空腹静脉采血检测血糖、甘油三酯、总胆固醇等.经颅多普勒超声(TCD)检测双侧椎动脉颅内段(VA)和基底动脉(BA)狭窄情况.用SPSS 11.0软件包进行数据统计分析.结果 1035名有效研究对象中,58例(5.6%)存在椎-基底动脉颅内段狭窄.其中左、右侧VA狭窄分别为17例和23例,BA狭窄30例.单因素分析提示,糖尿病患者中椎-基底动脉颅内段狭窄的患病率(10.3%)显著高于非糖尿病患者(3.2%,χ2=6.221,P=0.013);狭窄组人群平均收缩压水平[(131.1±25.5)mm Hg,1 mm Hg=0.133 kPa]显著高于非狭窄组[(124.1±21.6)mm Hg,t=2.228,P=0.026].Logistic回归分析证实糖尿病史和收缩压是椎-基底动脉颅内段狭窄的独立危险因素(糖尿病史:OR=3.305,P=0.023;收缩压升高1 mm Hg,OR=1.012,P=0.047).结论 椎-基底动脉颅内段狭窄在我国成年人群中均有较高的发生率.收缩压的升高和糖尿病是椎-基底动脉颅内段狭窄的重要危险因素.     

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 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.     

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.     

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.