老年脑白质疏松发病危险因素及对其认知功能的影响

目的探讨老年人发生脑白质疏松的危险因素及脑白质疏松对老年人认知功能的影响。方法选取2013-10—2016-11郑州市第九人民医院43例脑白质疏松患者为研究组,另选取同期体检健康者43例为对照组。统计2组糖尿病、高血压、高血脂、饮酒、吸烟、慢性阻塞性肺疾病等基本情况,抽取所有患者空腹静脉血4mL,以血糖分析仪测定空腹血糖、血脂、纤维蛋白原等实验室指标水平。统计分析脑白质疏松发病危险因素、危险因素与脑白质疏松病情相关性及2组认知功能(MMSE、MoCA)评分。结果年龄、糖尿病、高血压及纤维蛋白原水平均是脑白质疏松发病的影响因素(P0.05),Logistic回归分析可知,年龄、糖尿病、高血压及纤维蛋白原水平均是脑白质疏松发病的独立危险因素(P0.05)。Spearman检验可知,脑白质疏松发病危险因素年龄、糖尿病、高血压及纤维蛋白原水平均与脑白质疏松呈明显正相关关系(P0.05)。研究组MMSE评分(22.53±3.48)分、MoCA评分(23.01±3.50)分低于对照组[(28.04±0.89)分、(28.13±0.90)分],差异有统计学意义(P0.05)。结论脑白质疏松可对老年患者认知功能产生一定损害,年龄、糖尿病、高血压及纤维蛋白原水平均是导致脑白质疏松发生的独立危险因素,且其与患者病情存在明显正相关关系,临床可通过对上述危险因素进行积极干预防治脑白质疏松。     

血清胆红素和纤维蛋白原浓度与血管性认知损害非痴呆的相关性

目的探究血管性认知损害非痴呆(vascular cognitive impairment with no dementia,VCIND)患者血清胆红素和血浆纤维蛋白原(fibrinogen,FIB)浓度与认知功能的关系。方法测定82例VCIND组和70例对照组血浆纤维蛋白原和血清胆红素的浓度;采用简易精神状态检查量表(mini-mental state examination,MMSE)、蒙特利尔认知评估量表(Montreal cognitive assessment,MoCA)对入组者行神经心理学评价;比较两组间胆红素和纤维蛋白原浓度及认知功能变化情况;用Logistic回归法分析VCIND的影响因素。结果 VCIND组患者的血清胆红素浓度较对照组降低,而血浆FIB浓度较对照组明显升高;VCIND组MMSE评分(25.40±2.33)和MoCA评分(22.40±2.08)较对照组(28.44±1.11、27.44±1.04)偏低,差别均有统计学意义(t=-8.368,P=0.000;t=-10.644,P=0.000);血清胆红素水平与MMSE评分和MoCA评分总得分(r=0.271,P=0.042;r=0.341,P=0.009)及其子项目中的视空间与执行功能、注意力、延迟回忆等评分均呈正相关(r=0.322,P=0.024;r=0.232,P=0.034;r=0.307,P=0.005),血浆FIB水平与MMSE评分和MoCA总评分(r=-0.538,P=0.001;r=-0.464,P=0.007)及其子项目中的视空间与执行功能、注意力、延迟回忆、抽象思维等评分均呈负相关(r=-0.321,P=0.013;r=-0.305,P=0.016;r=-0.376,P=0.003;r=-0.295,P=0.017);Logistic回归分析显示:在调整多种因素后,高龄和高纤维蛋白原水平与认知功能为负性相关关系(β=0.115,P=0.001;β=2.818,P=0.000),高教育程度和总胆红素水平与与认知功能为正性相关关系(β=-0.281,P=0.000;β=-0.101,P=0.035)。结论 VCIND患者血清胆红素浓度下降,与认知功能呈正相关;血浆FIB升高,与认知功能呈负相关。较高年龄及纤维蛋白原水平是VCIND的危险因素,而较高的受教育程度及总胆红素水平是保护性因素。     

进展性大动脉粥样硬化型脑梗死的危险因素分析

目的探讨中国缺血性脑卒中亚型(CISS)分型中大动脉粥样硬化型(LAA)脑梗死病情进展的危险因素。方法前瞻性收集急性LAA脑梗死患者,根据美国国立卫生研究院卒中量表(NIHSS评分)评估患者病情是否进展,对可能影响患者病情进展的因素进行统计分析。结果共纳入351例患者,其中进展组112例(31.91%),非进展组239例(68.09%)。单因素分析2组患者高血压病史、饮酒史、空腹血糖、白细胞总数、纤维蛋白原水平、入院时收缩压及舒张压、入院时NIHSS评分、颅内外血管重度狭窄/闭塞、肺部感染、泌尿系感染、电解质紊乱有明显差异(P0.1),多因素Logistic逐步回归分析显示入院时收缩压、白细胞总数、颅内外血管重度狭窄/闭塞、纤维蛋白原水平、肺部感染、相较于轻度神经功能缺损的中度及重度神经功能缺损是进展性LAA脑梗死的独立危险因素。结论入院收缩压增高、白细胞总数增高、颅内外血管重度狭窄/闭塞、纤维蛋白原水平增高、肺部感染、中度及重度神经功能缺损是进展性LAA脑梗死的独立危险因素。     

无症状大脑中动脉狭窄患者脑白质改变进展的危险因素

目的对一项随机研究进行分析,探讨无症状大脑中动脉狭窄患者脑白质改变(white matter changes,WMC)发生和进展的危险因素。方法对无中风症状,但存在动脉硬化危险因素的患者进行磁共振检查,入选大脑中动脉(middle cerebral artery,MCA)狭窄的患者。记录临床特点和基础血生化指标,随访2年,随访结束时再次行磁共振检查。WMC采用定量分析,体积增加超过所有患者WMC体积增加的平均值被定义为有进展。Logistic回归分析确定WMC发生和进展的独立危险因素。结果 220例无症状MCA狭窄者患中,69例存在WMC,Logistic回归分析显示年龄(OR=1.096,P0.001)和高血压(OR=2.370,P=0.024)是WMC发生的独立危险因素。在进入研究时,69例的WMC平均体积为4.23cm3,经过两年时间增加至5.49cm3,有6例未能完成随访。随访结束时发现63例中24例(38.1%)WMC有进展。Logistic回归分析发现仅有基础WMC体积是预测WMC进展的独立危险因素(OR=1.329,P=0.003)。结论年龄和高血压是WMC发生的独立预测因素,而对于WMC的进展则是基础WMC体积更有预测意义,也就是说发现时WMC越严重,进展的机会越多,尽早发现WMC可能对于预防进展更有意义。     

青年脑梗死患者远期认知功能障碍的相关因素分析

目的筛选青年脑梗死患者远期认知功能障碍的相关因素。方法选择2008年1月至2013年6月在我院就诊的青年脑梗死患者58例,根据远期随访蒙特利尔认知量表(Mo CA)评分分为认知功能正常组和认知功能障碍组,比较两组患者的人口学、病情资料和活动功能,从中筛选出青年脑梗死患者远期认知功能障碍的危险因素。结果共有42例患者完成随访,平均随访时间为5.5年(3.3~7.1年),总体Mo CA评分(27.4±3.7)分。认知功能正常组18例,认知功能损害组24例,两组在性别、教育程度、TOAST分型、伴随疾病及嗜好、是否接受溶栓治疗进行组间比较,差异无统计学意义(P0.05)。认知功能障碍组的发病时年龄、美国国立卫生研究院卒中量表(NIHSS)评分大于认知功能正常组;左前循环梗死、出院时Rankin修订量表评分(mRS)2、复诊时工具性日常生活活动能力量表(IADL)8比例均高于认知功能正常组(P0.05)。经多因素Logistic回归分析得出,入院时NIHSS评分、左前循环梗死、出院时mRS2、复诊时IADL8均为认知功能障碍的独立危险因素(OR=1.039,4.329,5.143,12.800,21.333;P0.05)。结论入院时NIHSS评分左前循环梗死、出院时mRS2、复诊时IADL8是青年脑梗死患者远期认知功能障碍的危险因素;而认知功能与入院时NIHSS评分呈负相关。     

急性缺血性卒中后认知功能障碍及其相关因素的横断面研究

研究背景急性缺血性卒中可导致认知功能障碍,甚至引起血管性痴呆,早期识别血管性认知损害、积极寻找相关因素、及时进行有效治疗可以减少甚至防止认知功能进一步减退,本研究旨在探讨急性缺血性卒中后认知功能障碍及其相关因素。方法选择符合入组条件的急性缺血性卒中患者共314例,分别应用蒙特利尔认知评价量表(MoCA)评价认知功能、美国国立卫生研究院卒中量表(NIHSS)评价脑卒中后神经功能缺损程度、Barthel指数评价日常生活活动能力、汉密尔顿抑郁量表(HAMD)评价情绪状态。结果与脑卒中后无认知功能障碍组相比,脑卒中后认知功能障碍组患者受教育程度低、日常生活活动能力差(P=0.000,0.008),而HAMD评分和NIHSS评分增加(均P=0.000),血清超敏C反应蛋白和糖化血红蛋白水平升高(P=0.002,0.005);其中血清超敏C反应蛋白和糖化血红蛋白水平、NIHSS评分、HAMD评分与MoCA评分呈负相关(均P<0.05),Barthel指数与MoCA评分呈正相关(P<0.05);影像学分型以皮质型缺血性脑血管病和左侧大脑半球缺血性脑血管病为主(P<0.05)。Logistic回归分析提示,受教育程度低、糖尿病病史、HAMD评分、血清超敏C反应蛋白和糖化血红蛋白水平是脑卒中后认知功能障碍的危险因素。结论脑卒中后认知损害与社会人口学因素、脑卒中部位、抑郁程度、神经功能缺损程度,以及血清超敏C反应蛋白水平、血糖控制情况密切相关。     

高龄人群轻度认知功能损害的影响因素分析

目的探讨高龄人群轻度认知功能损害的影响因素。方法我院于2010-02—2013-11对高龄人群较为集中的多个社区老年人进行蒙特利尔认知功能量表(MocA)评定,并对评分符合轻度认知功能损害的245例患者进行一般情况调查,对相关影响因素进行统计分析。结果 2组年龄、性别、文化程度、经济收入、性格特征、饮食状况、参加社区活动情况以及有无业余爱好差异有统计学意义(P0.05)。进一步Logistic回归分析显示,性别、年龄、文化程度以及基础病是老年MIC的独立危险因素(P0.05)。结论老年女性、年龄增长、文化程度低下是影响高龄人群并发轻度认知功能损害的独立危险因素,临床可以此作为制定相应防治措施的依据。     

中至重型颅脑创伤患者多次输血影响因素分析

目的分析中至重型颅脑创伤患者多次输血影响因素。方法 2018年1月至2019年6月行去骨瓣减压术的53例中至重型颅脑创伤患者,根据凝血功能、血小板计数和临床表现(如有无创面渗血)确定是否输血;采用单因素和多因素Logistic回归分析筛查造成反复多次输血的危险因素。结果根据输血次数分为多次输血组(11例)和对照组(未输血或仅术中单次输血,42例)。多次输血组患者凝血酶时间(P=0.041)、国际标准化比值(P=0.048)、纤维蛋白降解产物(P=0.000)和D-二聚体(P=0.001)水平均高于对照组,纤维蛋白原低于对照组(P=0.006);Logistic回归分析显示,纤维蛋白降解产物是颅脑创伤患者反复多次输血的危险因素(OR=1.013,95%CI:1.005～1.021;P=0.002)。结论血清纤维蛋白降解产物水平升高是造成中至重型颅脑创伤患者反复多次输血的主要危险因素。     

帕金森病患者出现认知功能障碍的危险因素Logistic回归分析

目的探讨帕金森病患者出现认知功能障碍的危险因素,为临床预防提供参考。方法对97例帕金森病患者采用帕金森病统一评价量表(UPDRS)、蒙特利尔认知评估量表(MoCA)、汉密尔顿抑郁量表(HAMD)、H-Y分级量表调查,检测患者血尿酸、血浆同型半胱氨酸的水平。分析引起认知功能障碍发生的危险因素。结果 MoCA调查显示帕金森病患者认知功能障碍发生率69.07%;无认知功能障碍组受教育年限、血尿酸高于认知功能障碍组(P0.05),病程、MAMD评分、H-Y分级、PUDRSⅡ评分、PUDRSⅢ评分、血浆同型半胱氨酸均低于认知功能障碍组(P0.05或P0.01);多因素Logistic回归分析显示,受教育年限、病程、MAMD评分、H-Y分级、PUDRSⅢ评分与患者发生认知功能障碍关系密切,是独立危险因素(P0.05或P0.01)。结论受教育年限、病程、MAMD评分、H-Y分级、PUDRSⅢ评分是帕金森病患者出现认知功能障碍的相关危险因素,应加以关注。     

急性缺血性卒中后认知功能障碍危险因素分析

目的探讨急性缺血性卒中(AIS)后认知功能障碍的危险因素。方法应用简易精神状态检查量表(MMSE)评定AIS患者发病后14d的认知功能,根据MMSE评分将患者分为认知障碍组与非认知障碍组,比较两组年龄、性别、血管危险因素、临床检验资料等。采用多变量Logistic回归分析AIS后认知功能障碍的独立危险因素。结果 (1)共纳入AIS患者163例,其中认知障碍组72例(44.17%),非认知障碍组91例(55.83%);(2)认知障碍组年龄73.3±8.2岁vs 62.8±10.3岁,(t=7.11,P<0.001)、高血压83.3%vs 52.7%,(χ~2=15.48,P<0.001)、糖尿病65.3%vs 25.3%,(χ~2=24.65,P<0.001)、卒中或短暂性脑缺血发作史70.8%vs 36.3%,(χ2=17.81,P<0.001)的比例、三酰甘油1.3(1,1.9)mmol·L~(-1)vs1.1(0.9,1.5)mmol·L~(-1)),(P=0.038)、血低密度脂蛋白3.8(3,4.6)mmol·L~(-1) vs 2.9(2.4,3.6)mmol·L~(-1)),(P<0.001)、尿酸383.4(295.1,445.4)mmol·L~(-1) vs 320.7(263.6,376.4)mmol·L~(-1),(P=0.002)和C反应蛋白7.7(3.7,12.6)mmol·L~(-1) vs 1.9(0.7,6.4)mmol·L~(-1),(P<0.001)水平均显著高于非认知障碍组;(3)多变量Logistic回归分析显示,年龄优势比(OR)1.13,95%可信区间(CI)1.08~1.18,(P<0.001)、糖尿病(OR)5.56,95%CI 2.82~10.95,(P=0.003)、卒中或短暂性脑缺血发作史(OR)4.27,95%CI 2.2~8,29,(P=0.002)、血清低密度脂蛋白(OR)2.07,95%CI 1.46~2.93,(P<0.001)水平增高为AIS后认知损害的独立危险因素。结论 AIS后的认知功能障碍发病率高;年龄、糖尿病、卒中或短暂性脑缺血发作病史以及血低密度脂蛋白为AIS后发生认知功能障碍的独立危险因素。     

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.     

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.     

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.     

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.     

The influence of comorbid depression on seizure severity

PURPOSE: To determine the relation between depressive symptoms and seizure severity among people with epilepsy. METHODS: A postal questionnaire was used to survey a nationwide community sample about seizures and depression. The Seizure Severity Questionnaire (SSQ) assessed the severity and bothersomeness of seizure components. The Centers for Epidemiological Studies-Depression scale categorized levels of depression. RESULTS: Respondents categorized as having current severe (SEV, n = 166), mild-moderate (MOD, n = 74), or no depression (NO, n = 443) differed significantly in SSQ scores (all p < 0.0001). People with SEV or MOD reported significantly worse problems than did those with NO depression for overall seizure recovery (mean, 5.3, 4.9, 4.5, respectively); overall severity (5.0, 4.5, 4.2); and overall seizure bother (5.3, 4.8, 4.4) (all p < 0.005). Cognitive, emotional, and physical aspects of seizure recovery also were rated worse among people with SEV than with NO depression (all p < 0.05). Symptoms of depression were significantly correlated with higher levels of all components of generalized tonic-clonic seizure severity (r = 0.33-0.48; all p < 0.0001), and partial seizures (r = 0.31-0.38; all p < 0.01). CONCLUSIONS: Clinically depressed people with epilepsy reported higher levels of perceived severity and bother from seizures, as well as greater problems with overall seizure recovery than did nondepressed people experiencing similar types of seizures. The pervasive influence of depressive symptoms on reports of seizure activity suggests that people with epilepsy should be screened for depression. These data highlight the importance of detecting and treating depression among people with epilepsy.     

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.