中性粒细胞脱颗粒因子及中性粒细胞与淋巴细胞的比值对大面积脑梗死脑疝的预测价值及短期预后的影响

目的 检测大面积脑梗死（massive cerebral infarction,MCI）患者外周血中中性粒细胞脱颗粒因子［髓过氧化物酶（myeloperoxidase, MPO）、中性粒细胞弹性蛋白酶（neutrophil elastase,NE）、细胞纤连蛋白（cellular fibronectin,cFn）、尿激酶纤溶酶原激活物受体（urokinase-type plasminogen activator receptor,uPAR）］及中性粒细胞与淋巴细胞的比值（neutrophil-to-lymphocyte ratio,NLR）的水平,分析其对MCI患者发生脑疝的预测价值及短期预后的影响。方法 收集2018年1月至2021年12月住院治疗的MCI患者95例,根据MCI发病5 d内是否合并脑疝将患者分为非脑疝组（32例）和脑疝组（63例）。随访期间失访8例。根据随访时改良Rankin量表（modified Rankin Scale,mRS）评分将患者分为预后良好组（18例,mRS评分≤2分）和预后不良组（69例,mRS评分>2分）。分析美国国立卫生研究院卒中量表（National Institutes of Health Stroke Scale,NIHSS）评分与NLR、MPO和NE水平的相关性。采用多因素Logistic回归分析探讨MCI患者发生脑疝的危险因素。采用受试者操作特征曲线评估NLR和MPO预测脑疝发生的临床价值。比较预后良好组和预后不良组NLR和MPO水平。结果 脑疝组与非脑疝组相比,去骨瓣减压术患者比例、白细胞计数、中性粒细胞计数及NLR、MPO、NE、cFn和uPAR水平之间差异有统计学意义（P<0.05）。NIHSS评分与NLR、MPO和NE均呈正相关（分别r=6.524、6.895、7.236,均P<0.05）。NLR和MPO为影响MCI患者发生脑疝的危险因素（OR=2.361,P=0.007;OR=2.955,P=0.014）。NLR预测MCI患者发生脑疝的曲线下面积为0.914（95%CI：0.875~0.921）,高于MPO预测MCI患者发生脑疝的曲线下面积［0.817（95%CI：0.802~0.856）;Z=4.201,P=0.008］。预后良好组的NLR和MPO水平均低于预后不良组（P<0.001）。结论 MCI患者入院时NLR和MPO的水平为影响脑疝发生的危险因素;NLR预测MCI患者发生脑疝的临床价值高于MPO;NLR和MPO水平与MCI患者预后有关。 [国际神经病学神经外科学杂志, 2023, 50(2): 23-28]     

青少年抑郁障碍患者与双相情感障碍患者睡眠特征及其对自杀风险的影响

目的 比较青少年抑郁障碍患者和双相情感障碍患者睡眠结构特征的差异,探讨睡眠指标等因素对患者自杀风险的影响。方法 回顾性查阅广州医科大学附属脑科医院2019年1月1日-2021年6月30日符合《国际疾病分类（第10版）》（ICD-10）诊断标准的抑郁障碍（n=97）和双相情感障碍（n=52）住院青少年患者病历资料,收集患者的年龄、性别、体质量指数（BMI）、精神科诊断、自杀风险评估量表（NGASR）评分及多导睡眠监测（PSG）结果。根据NGASR评分结果,将患者分为两组：0~5分为自杀低风险组（n=32）,>5分为自杀高风险组（n=117）。以既往文献中80例正常青少年的PSG数据作为对照组资料。建立多元线性回归模型探讨青少年情感障碍患者自杀风险的影响因素。结果 自杀高风险组睡眠效率和N2期睡眠占比均低于自杀低风险组（Z=-2.138、-2.520,P均<0.05）。抑郁组总睡眠时间、N2期睡眠时间以及REM期睡眠时间均少于双相组（t=-2.822、-3.087、-2.277,P<0.05或0.01）;抑郁组和双相组REM期睡眠占比均低于对照组（t=-2.369、-2.069,P均<0.05）。线性回归分析显示,青少年情感障碍患者自杀风险的影响因素包括N1期睡眠时间（β=0.019,P<0.05）、性别（男性vs.女性,β=-4.051,P<0.01）以及诊断（双相情感障碍vs.抑郁障碍,β=-1.429,P<0.05）。结论 与青少年双相情感障碍患者相比,青少年抑郁障碍患者存在睡眠连续性差、浅睡眠更少的特点。N1期睡眠时间、女性以及诊断为抑郁障碍是青少年情感障碍患者自杀的影响因素。     

伴失眠的抑郁症患者睡眠认知特征及其对睡眠质量的影响

目的 了解伴失眠的抑郁症患者对睡眠的信念与态度，并探讨其对睡眠质量的影响。方法 纳入在首都医科大学附属北京安定医院就诊、符合《精神障碍诊断与统计手册（第4版）》（DSM-IV）诊断标准的伴失眠的抑郁症患者（n=61）和原发性失眠患者（n=62）为研究对象，并招募健康对照组（n=64）。三组被试均接受睡眠功能失调信念和态度量表（DBAS）及匹兹堡睡眠质量指数量表（PSQI）评定，伴失眠的抑郁症患者同时接受汉密尔顿抑郁量表17项版（HAMD-17）评定。采用协方差分析比较三组被试PSQI和DBAS评分。采用多元线性回归分析探讨伴失眠的抑郁症患者PSQI评分的影响因素。结果 伴失眠的抑郁症组和原发性失眠组PSQI评分均高于对照组（t=18.932、18.610，P均<0.01），两组DBAS评分均低于对照组（t=-5.561、-5.791，P均<0.01）。以伴失眠的抑郁症患者PSQI评分作为因变量，建立的多元线性回归方程具有统计学意义（F=14.095，R²=0.327，P<0.05），DBAS中对睡眠的预测与控制因子和年龄是患者睡眠质量的影响因素（B=-0.100、-0.279，P<0.05或0.01）。结论 伴失眠的抑郁症患者比正常人存在更多的睡眠相关负性认知，且不良认知可能是其睡眠质量的影响因素。     

重度颅脑损伤术后并发脑疝的危险因素分析及预警性干预建议

目的 分析重度颅脑损伤术后并发脑疝的危险因素。方法 对安徽医科大学附属宿州医院2018年6月—2021年6月收治的120例重度颅脑损伤患者的临床资料进行回顾性分析，并统计脑疝发生率和死亡率，分析并发脑疝的危险因素。结果 术后并发脑疝33例，脑疝发生率27.50%，且并发组和未并发组死亡率分别为27.27%和11.49%，差异有统计学意义（χ²=4.470，P=0.035）；多因素Logistic回归分析结果显示，年龄＞60岁、吸烟史、术前GCS≤6分、合并心房颤动、合并低钠血症、术前基底池受压、术后甘露醇半量、腰椎穿刺、术后并发颅内血肿为并发脑疝的危险因素（均P＜0.05）。结论 重度颅脑损伤患者术后并发脑疝风险较高，危险因素较多，需要加强预警，及时进行干预。 [国际神经病学神经外科学杂志, 2023, 50(4): 25-28]     

社区精神分裂症患者代谢综合征影响因素

背景 精神分裂症患者是罹患代谢综合征的高风险人群。既往关于代谢综合征影响因素的研究主要集中于住院精神分裂症患者,对社区精神分裂症患者的研究较少。目的 探索广州市社区精神分裂症患者不同代谢综合征风险层级的影响因素,为社区精神分裂症患者代谢综合征干预提供参考。方法 于2021年11月,选取广州市精神卫生信息系统在册在管且完成2020年度健康体检的精神分裂症患者3 339例。从信息系统导出患者健康体检资料,采用《中国2型糖尿病防治指南（2020年版）》评估患者是否罹患代谢综合征。根据《精神分裂症患者代谢综合征管理的中国专家共识》,将患者分为高风险组（n=423）、临界组（n=1 524）和代谢综合征组（n=1 392）。采用多元Logistic回归分析社区精神分裂症患者罹患代谢综合征的危险因素。结果 社区精神分裂症患者代谢综合征患病率为41.69%。单因素分析显示,三组在性别（χ²=44.610）、年龄（χ²=55.992）、婚姻状况（χ²=30.755）、病程（χ²=25.913）和体质量指数（χ²=829.265）方面差异均有统计学意义（P均<0.01）。Kruskal-Wallis H检验显示,三组患者腰围（H=920.331）、收缩压（H=436.673）、舒张压（H=393.337）、空腹血糖（H=807.304）、甘油三酯（H=1 134.125）、高密度脂蛋白胆固醇（H=593.615）水平差异均有统计学意义（P均<0.01）。Logistic回归分析显示,年龄≥50岁（OR=1.761,95% CI：1.087~2.853）、超重（OR=2.418,95% CI：1.862~3.140）和肥胖（OR=57.903,95% CI：14.340~233.802）是社区精神分裂症患者成为代谢综合征临界人群的危险因素（P<0.05或0.01）;女性（OR=1.295,95% CI：1.034~1.622）、年龄40~49岁（OR=2.597,95% CI：1.582~4.263）、年龄≥50岁（OR=4.392,95% CI：2.609~7.395）、超重（OR=7.844,95% CI：6.018~10.223）和肥胖（OR=426.785,95% CI：105.724~1 722.839）是社区精神分裂症患者成为代谢综合征人群的危险因素（P<0.05或0.01）。结论 社区精神分裂症患者代谢综合征患病率较高,女性、年长、超重和肥胖是精神分裂症患者罹患代谢综合征的高风险因素。     

医学生偏头痛患者睡眠时间不足的发生率及影响因素分析

目的 调查医学生偏头痛患者睡眠时间不足的发生率及影响因素，为改善睡眠质量提供参考。方法 采用整群抽样方法，于2018年7月-2019年7月选取川北医学院在校医学生中符合《国际头痛疾病分类（第3版）》（ICHD-3）偏头痛诊断标准的546名患者为研究对象，并根据每夜睡眠时间是否>6 h分为睡眠时间充足组（n=367）与睡眠时间不足组（n=179）。收集医学生一般人口学资料及临床资料，采用匹兹堡睡眠质量指数量表（PSQI）评定睡眠情况，采用汉密尔顿焦虑量表（HAMA）和汉密尔顿抑郁量表24项版（HAMD-24）评定焦虑抑郁情况，采用视觉模拟评分法（VAS）和头痛影响测试量表（HIT-6）评定头痛严重程度及其对日常生活的影响。采用Logistic回归分析探索偏头痛患者睡眠时间不足的影响因素。结果 在546名医学生偏头痛患者中，有179人（32.78%）存在睡眠时间不足。睡眠时间不足组和睡眠时间充足组的年龄（t=2.107）、头痛频率（Z=-2.972）、焦虑状态（χ2=14.053）、抑郁状态（χ2=10.773）、PSQI评分（t=-13.247）及睡眠质量（χ2=94.754）差异均有统计学意义（P?0.05或0.01）。相关分析显示，偏头痛患者睡眠时间与年龄呈负相关（r=-0.100，P<0.01），与头痛频率、焦虑状态、抑郁状态呈正相关（r=0.135、0.169、0.139，P均<0.01）。多因素Logistic回归分析显示，年龄（OR=0.860，95% CI：0.743~0.996，P=0.045）、头痛频率（OR=1.051，95% CI：1.006~1.098，P=0.026）、抑郁状态（OR=1.712，95% CI：1.024~2.861，P=0.040）是医学生偏头痛患者睡眠时间不足的影响因素。结论 医学生偏头痛患者睡眠时间不足的发生率较高，头痛频率高和抑郁状态是其危险因素，年龄是保护因素。     

儿童青少年精神障碍患者睡眠不足及相关因素

目的 探讨儿童青少年精神障碍患者睡眠不足的现况及相关影响因素。方法 选取2021年2月-6月就诊于阜阳市第三人民医院且符合《国际疾病分类（第10版）》（ICD-10）精神分裂症、抑郁障碍、童年情绪障碍诊断标准的131例儿童青少年患者为研究对象，采用自制调查问卷收集患者的一般人口学资料、睡眠情况、生活情况、家庭和学校情况等信息，比较睡眠充足组和睡眠不足组人口学资料的差异，采用Spearman法分析患者睡眠不足的相关因素。结果 ①在131例儿童青少年精神障碍患者中，93例（71.0%）存在睡眠不足，睡眠不足组与睡眠充足组在疾病类别（χ²=8.798，P=0.012）、近6个月内被打（χ²=3.427，P=0.035）或被骂（χ²=4.145，P=0.031）以及一年内遭受网络欺凌（χ²=4.187，P=0.041）方面，差异均有统计学意义。②在睡眠不足的患者中，77例（82.8%）存在入睡困难，69例（74.2%）存在夜间多醒。③儿童青少年精神障碍患者睡眠不足与近6个月内有被骂经历（r=0.210，P=0.037）或被打经历（r=0.145，P=0.023）以及一年内遭受网络欺凌（r=0.179，P=0.041）呈正相关。结论 儿童青少年精神障碍患者睡眠不足的发生风险较高，且与抑郁障碍、有被打和被骂经历、经受过网络欺凌相关。     

血清可溶性CD40配体与急性脑梗死患者颈动脉斑块的关系

目的 探讨血清可溶性CD40配体（sCD40L）水平与急性脑梗死患者颈动脉粥样硬化斑块的关系。方法 选取2018年5月至2019年5月在中国医科大学附属盛京医院神经内科住院的急性脑梗死患者108例。根据颈部动脉超声结果分为无斑块组和斑块组，斑块组根据斑块性质进一步分为稳定斑块组和不稳定斑块组。应用酶联免疫吸附法（ELISA）测定血清sCD40L水平；分析血清sCD40L水平与颈动脉粥样硬化斑块的关系。结果 颈动脉斑块组患者高血压（P=0.026）、空腹血糖（P=0.045）、三酰甘油（P=0.027）、低密度脂蛋白胆固醇（LDL-c）（P=0.005）和sCD40L水平（P<0.001）均高于无斑块组。高血压（OR=2.598，P=0.028）、LDL-C（OR=4.247，P=0.006）和sCD40L水平（OR=1.079，P=0.009）是急性脑梗死患者存在颈动脉粥样硬化斑块的危险因素。颈动脉不稳定斑块组患者高血压（P=0.031）、白细胞计数（P=0.002）、低密度脂蛋白胆固醇（P=0.003）和sCD40L水平（P<0.001）均高于稳定斑块组。不稳定颈动脉斑块组患者，高血压（OR=2.918，P=0.033）和sCD40L水平（OR=2.712，P<0.001）是急性脑梗死患者颈动脉斑块不稳定性的危险因素。结论 急性脑梗死患者血清sCD40L水平的升高与颈动脉粥样硬化斑块的发生和发展相关，亦与颈动脉斑块的不稳定性相关。     

伴中重度阻塞性睡眠呼吸暂停低通气综合征的抑郁症患者多导睡眠监测特点

目的 探讨伴中重度阻塞性睡眠呼吸暂停低通气综合征（OSAHS）的抑郁症患者多导睡眠监测（PSG）特点。方法 回顾性分析2017年12月-2019年10月在苏州市广济医院睡眠医学中心完成整夜多导睡眠监测（PSG）的门诊和住院患者以及健康体检人群,从中筛选出四组被试,分别为伴中重度OSAHS的抑郁症患者（n=31）、不伴OSAHS的抑郁症患者（n=79）、中重度OSAHS患者（n=96）和正常对照组（n=32）。比较四组被试睡眠进程相关指标（总睡眠时间、睡眠潜伏期、觉醒次数）和睡眠结构相关指标（N1、N2、N3期及REM期占总睡眠时间的比例,REM潜伏期、REM期持续时间）以及睡眠呼吸相关指标（氧减指数）等参数。结果 睡眠进程方面,四组被试总睡眠时间、睡眠潜伏期和觉醒次数差异均有统计学意义（F=2.874、3.959、12.291,P<0.05或0.01）。睡眠结构方面,四组被试N2期、N3期占总睡眠时间比例差异均有统计学意义（F=13.885、48.013,P均<0.01）;四组被试REM潜伏期、REM期持续时间、REM期占总睡眠时间比例差异均有统计学意义（F=41.492、11.827、10.552,P均<0.01）。睡眠呼吸相关指标方面,四组被试氧减指数差异有统计学意义（F=170.585,P<0.05）。结论 伴中重度OSAHS的抑郁症患者存在严重的睡眠进程和结构紊乱,同时伴有更频繁和更严重的呼吸相关事件。     

酒精使用障碍严重程度的影响因素及风险预测模型构建

背景 酒精使用障碍（AUD）是常见的慢性复发性精神疾病,对于重度AUD,需早期快速识别并及时妥善处理,以避免不可逆的伤害发生。目前,对AUD严重程度的评估主要基于临床医师对患者的精神检查,关于AUD严重程度影响因素及预测模型的研究有限。目的 分析AUD患者疾病严重程度的影响因素,构建风险预测模型,为评估AUD患者的疾病严重程度提供参考。方法 回顾性选取2017年1月1日—2022年12月31日南宁市第五人民医院收治的、符合《精神障碍诊断与统计手册（第5版）》（DSM-5）AUD诊断标准的1 358例首次住院患者为研究对象,收集其基本资料,根据疾病严重程度分为轻中度组（n=330）和重度组（n=1 028）。按7∶3将患者分为训练集和测试集,在训练集样本中构建Logistic回归模型,在测试集样本中采用受试者工作特征（ROC）曲线分析该模型对AUD严重程度的预测价值。结果 与轻中度组相比,重度组居住地在城市（χ²=7.804）、农民（χ²=17.991）、饮酒频率高于1~2次/天（χ²=35.267）的比例更高,初次饮酒年龄更大（t=-3.858）,合并躯体疾病数量更多（Z=-22.782）,γ-谷氨酰胺转移酶（χ²=259.940）和总胆红素异常（χ²=148.552）的比例更高（P均<0.01）。在训练集中进行的Logistic分析结果表明,农民（OR=2.024,95% CI：1.352~3.029）、初次饮酒年龄较大（OR=1.075,95% CI：1.025~1.129）、用餐时间外也饮酒（OR=3.988,95% CI：2.408~6.606）、总胆红素水平异常（OR=1.034,95% CI：1.000~1.069）、合并更多的躯体疾病（OR=4.386,95% CI：2.636~7.298）是AUD更严重的危险因素。该模型在测试集中的ROC曲线下面积（AUC）为0.906。结论 在精神专科医院中,农民、初次饮酒年龄较大、用餐时间外也饮酒、总胆红素水平异常、合并更多的躯体疾病可能是重度AUD的危险因素。     

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.     

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.     

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.