酒依赖患者的主观与客观睡眠质量比较

目的:比较酒依赖患者主观与客观睡眠质量。方法:60例男性酒依赖患者(患者组)根据其入组时是否完成急性戒酒治疗且维持4周戒酒分为饮酒亚组和戒断亚组,各30例;对其进行修订匹兹堡睡眠质量指数问卷(PSQI)评估及并多导睡眠图(PSG)检测,并在PSG结束时调查受试者的睡眠感受;结果与28名男性健康志愿者比较,分析各组主观与客观睡眠质量。结果:患者组PSQI总分及各成分评分显著高于对照组(P均0.01);饮酒亚组PSQI总分及各成分评分显著高于戒断亚组(P均0.01)。PSG检测结果:与对照组比较,患者组入睡潜伏期(SL)延长(P0.01),总睡眠时间(TST)减少(P0.01),觉醒次数(AN)增多(P0.01),慢波睡眠百分比(SWS)增加(P0.05),快眼动睡眠潜伏期(RL)延长(P0.05),快眼动睡眠时间(RT)减少(P0.01);与戒断亚组比较,除SL外,饮酒亚组TST减少(P0.01),AN增多(P0.01),SWS增加(P0.05),RL延长(P0.05),RT减少(P0.01)。各组内TST及SL主-客差异均有统计学意义(P0.05或P0.01);患者组TST及SL主观感显著差于PSG结果;与戒断亚组比较,饮酒亚组SL主观感要好于PSG结果。结论:酒依赖患者睡眠质量差,其主观感受也明显差于实际情况;戒酒后患者的睡眠质量要好于饮酒者,但急性期戒酒后患者主观感入睡困难更为明显。     

慢性原发性失眠患者主客观睡眠质量差异及相关因素

背景慢性失眠患者由于警觉性和浅睡比例较高,常判断不清入睡与觉醒的界限,表现为对失眠特别是入睡困难和睡眠时间不足的严重程度常有夸大,即使使用药物改善睡眠后也有同样的表现,而原发性失眠患者伴有明显的心身症状。因此我们观察患者主观与客观睡眠质量的差异与焦虑症状之间的关系,初步了解影响慢性原发性失眠患者主客观睡眠差异的相关因素。方法共收录慢性失眠患者55例,男24例,女31例。符合美国精神障碍诊断与统计手册第4版(DSM-IV)原发性失眠症诊断标准,采用病程超过6个月为慢性失眠。排除患有符合DSM-IV轴I障碍诊断标准的精神障碍者及明显躯体疾病者。收录正常对照组共15名,男8名,女7名。其中性别及年龄与患者组差异无统计学意义,排除有超过1周失眠主诉者及患有符合DSM-IV轴I精神障碍诊断标准的精神障碍者及明显躯体疾病者。所有受试者完成匹兹堡睡眠质量指数表(Pittsburgh sleep quality index,PSQI)、状态-特质焦虑问卷(STAI)、一般情况调查表及在多导睡眠仪监测前3d连续的睡眠日记;并在睡眠监测前晚进行一夜的预睡。结果①分析显示,秩和检验分析显示,慢性原发性失眠患者的无论主观或客观入睡潜伏期、睡眠时间及睡眠效率均小于正常对照组[分别是主观睡眠时间为(157.8±141.7)minv.s(423.4±42.8)min,P<0.001;客观睡眠时间为(332.2±154.7)minv.s(418.1±47.8)min,P=0.009;主观入睡潜伏期为(80.3±73.7)minv.s.(19.2±8.6)min,P<0.001;客观睡眠潜伏期为(23.2±25.4)minv.s.(7.7±4.7)min,P=0.017;主观睡眠效率为(0.52±0.27)v.s.(0.91±0.05),P<0.001;客观睡眠效率为(0.67±0.28)v.s.(0.90±0.07),P<0.001]。②秩和检验分析显示,慢性失眠患者主观睡眠潜伏期大于PSG监测值[(80.3±73.7)minv.s.(23.2±25.4)min,P<0.001],主观睡眠时间、睡眠效率低于PSG监测值[分别为(157.8±141.7)minv.s.(332.2±154.7)min,P<0.001;(0.52±0.27)v.s.(0.67±0.28),P<0.001];而正常对照组除在主、客观睡眠潜伏期存在差异[(19.2±8.6)minv.s.(7.7±4.7)min,P=0.019]外,其他观察值均无明显差异。③患者主观与客观睡眠潜伏期差值与STAI总分、TAI及SAI分呈正相关(r分别为0.402、0.374及0.397,P<0.05),而与病程、性别及年龄无明显相关性;主客观睡眠效率差值与STAI各项目分及病程、性别、年龄无显著相关性。结论慢性原发性失眠患者存在过分夸大失眠严重程度的倾向,主客观睡眠时间、睡眠效率与入睡潜伏期均有明显的差别,其主客观睡眠潜伏期的差异与患者的特质焦虑水平及状态焦虑水平呈正相关。提示焦虑症状在其主客观睡眠质量差异中起到关键的作用。     

米氮平治疗抑郁症患者的早期睡眠多导图改变

目的 通过睡眠多导图(PSG)客观评价米氮平治疗早期抑郁症伴失眠患者睡眠结构的影响及改善睡眠的疗效.方法 入组25例抑郁症伴失眠患者,在进行基线量表评估和PSG监测后开始服药,米氮平起始剂量每天15 mg,3 d后增至每天30 mg,睡前1 h服用;7 d后再次进行量表评估和PSG监测;观察治疗后失眠、焦虑抑郁症状、PSG的变化.结果 25例抑郁症伴失眠患者在米氮平治疗7 d后分别进行量表评分,显示各量表减分值分别为Athens失眠量表(7.92±3.86,t=10.255,P=0.000)、汉密尔顿抑郁量表(9.80±4.41,t=12.132,P=0.000)、汉密尔顿焦虑量表(6.84±5.57,t=6.137,P=0.000);PSG结果显示治疗总睡眠时间(min)延长(402.46±80.75,t=-2.990,P=0.006)、睡眠觉醒时间(min)缩短(80.38±48.02,t=2.972,P=0.007)、睡眠效率明显提高(76.17%±10.65%,t=-2.750,P=0.011),深睡眠比例显著增加(19.66%±11.43%,t=3.236,P=0.004),而入睡潜伏期和睡眠中清醒次数、快速眼动睡眠潜伏期、比例及出现次数无差异.结论 单一使用米氮平治疗抑郁症伴失眠患者起效快,同时能增加总睡眠时间、缩短睡眠觉醒时间、提高睡眠效率、增加深睡眠比例等,达到有效改善失眠.     

首发未服药的精神分裂症患者多导睡眠图特征

目的 探索首次发病的精神分裂症患者多导睡眠图(Polysomnography PSG)的特征.方法 对22例首发精神分裂症患者和18名正常对照进行整夜PSG监测,采用匹兹堡睡眠质量指数量表评估主观睡眠,比较两组PSG及主客观睡眠的差异.结果 与对照组比较,患者组表现入睡潜伏期延长[(67.26±13.02)min vs(28.73±10.47)min],总睡眠时间减少[(271.46±25.14)min vs (357.81±22.83)min]、睡眠效率下降[(61.58±11.62) vs (89.71±9.44)]、睡眠期觉醒时间[(67.84±13.76)min vs (26.94±8.67)min]和觉醒次数[(34.58±9.49) vs (13.46±4.03)]增多、N1期睡眠增加[(81.29±12.41)min vs (39.51±8.63)min],N2期、N3期睡眠减少[(94.23±16.53)min vs (162.84±18.93)min; (39.78±7.64)min vs (84.15±11.39)min],REM睡眠减少[(47.52±7.64)min vs (73.56±9.43)min],上述组间差异均有统计学意义(P<0.05).与PSG值比较,患者组主观评估睡眠潜伏期延长、睡眠时间减少、睡眠效率下降(P<0.05).结论 首发精神分裂症患者有睡眠连续性和睡眠结构两方面异常,且对失眠有主观夸大特征.     

失眠症患者睡眠质量的主观评估与多导睡眠图参数对比分析

目的 探讨失眠症患者对睡眠质量的主观评估,并通过对多导睡眠图(PSG)睡眠参数的定量分析,对失眠症患者的睡眠状况进行客观评估,进一步将二者进行对比分析.方法 对失眠症患者和健康人各100例运用匹兹堡睡眠质量指数问卷(PSQI)进行评定,并分别进行多导睡眠图的整夜睡眠描记,次日晨起后询问夜间睡眠情况.结果 失眠症组PSQI各成分得分及总分均高于对照组,差异有统计学意义(P＜0.01).与对照组相比,失眠症组的睡眠潜伏期(min)延长(失眠症组43.69±11.54,对照组16.01±10.44)、总睡眠时间(min)减少(失眠症组314.65±91.89,对照组446.41±77.81)、睡眠效率降低(失眠症组64.51%±18.59%,对照组91.32%±3.58%)、快眼动睡眠时间(min)减少(失眠症组33.26±15.61,对照组93.21±21.63),差异有统计学意义(P＜0.01).失眠症组对总睡眠时间的评估较PSG检测值显著减低、对睡眠潜伏期的评估较PSG检测值显著增高,自我评估与实际睡眠情况不一致.结论 失眠症患者睡眠质量较差.失眠症患者的PSG各睡眠参数有特征性的改变,利用PSG检查发现失眠症患者对失眠情况的主客观评估不一致,存在过高估价睡眠潜伏期和过低估价睡眠时间的倾向.     

超低频经颅磁刺激治疗缺血性脑卒中患者失眠的 临床疗效

目的 观察超低频经颅磁刺激（ILF-TMS）治疗缺血性脑卒中后失眠的临床疗效。方法 选 取60例缺血性脑卒中后失眠患者，按照随机数字表法将其分为常规治疗组（30例）和ILF-TMS治疗组（30 例）， 两组患者均口服酒石酸唑吡坦片，每晚睡前口服5 mg。ILF-TMS 治疗组在此基础上加用ILF-TMS 治疗， 常规治疗组每日接受伪ILF-TMS治疗，患者治疗前和治疗后（10 d 后）均给予匹兹堡睡眠质量指数（PSQI） 和多导睡眠图（PSG）相关参数评价睡眠情况，PSG 评价参数主要包括总睡眠时间（TST）、睡眠潜伏期（SL） 以及睡眠NREM（S1、S2、S3 +S4 ）、REM 的睡眠结构比。结果 治疗前两组患者PSQI、TST、SL、S1、S2、 S3+S4、REM 评分比较，差异无统计学意义（P＞ 0.05）。常规治疗组患者10 d 后PQSI评分较前明显降低 ［（18.03±1.37）分比（12.60±2.43）分］；TST 较前明显延长［（251.42±42.42）min 比（288.80±40.32）min］； SL 较治疗前有显著缩短［（39.60±17.62）min 比（34.40±14.89）min］，差异均有统计学意义（P ＜ 0.05），睡 眠结构S1、S2、S3+S4、REM 较治疗前均无明显变化。ILF-TMS 治疗组患者10 d 后PQSI评分较前明显降 低［（18.17±1.29）分比（10.40±2.13）分］；TST较前明显延长［（241.50±51.75）min 比（353.45±52.20）min］； SL 较治疗前有显著缩短［（40.80±17.47）min 比（26.60±13.22）min］，差异均有统计学意义（P ＜ 0.05），而 睡眠结构S1、S2、S3+S4、REM 较治疗前均无明显变化。与常规治疗组比较，ILF-TMS 治疗组患者治疗后 PSQI评分更低，TST更长，SL更短，差异均有统计学意义（P＜ 0.05）。结论 ILF-TMS 可以改善缺血性脑 卒中后失眠症状，短期（10 d）ILF-TMS 治疗尚不能改善缺血性脑卒中后失眠患者的睡眠结构。     

失眠症患者睡眠质量及多导睡眠图研究

目的调查分析失眠症患者主、客观睡眠状况及睡眠质量。方法采用睡眠状况自评量表和多导睡眠图监测仪对27例失眠症患者和20例正常对照组分别进行睡眠质量评定和整夜多导睡眠图描记,次日晨完成早晨问卷。结果失眠症组睡眠问题多于对照组(P<0.01)。失眠症组总睡眠时间(TST),睡眠效率、REM睡眠时间、睡眠维持率、N3时间、N3%均低于对照组(P<0.05或0.01),睡后觉醒时间、觉醒次数、N2%、觉睡比、微觉醒总时间均高于对照组(P<0.01)。失眠症组入睡困难因子与睡眠维持率负相关(r=-0.44,P<0.05),与微觉醒总时间正相关(r=0.49,P<0.05);服药情况因子与觉醒次数、睡眠潜伏期、REM潜伏期、N2时间及N2%正相关(r=0.41～0.66,P<0.05或0.01),与REM睡眠时间及比例、N3时间及N3%负相关(r=-0.53～-0.41,P<0.05或0.01)。SRSS总分与N2%正相关(r=0.47,P<0.05),与睡眠维持率负相关(r=-0.41,P<0.05)。失眠症组的主观睡眠潜伏期大于客观睡眠潜伏期(P<0.01),主观总睡眠时间少于客观睡眠时间(P<0.01),而对照组主客观睡眠潜伏期、睡眠时间差异均无统计学意义(P>0.05)。结论失眠症患者的睡眠质量比较差,存在入睡过长、频繁觉醒、深睡眠及REM睡眠减少等睡眠问题。同时对自身睡眠状况的评价存在主、客观的不平衡,失眠症患者有过分估计自己失眠的特点。     

重复经颅磁刺激治疗焦虑症伴失眠的临床疗效

目的探讨重复经颅磁刺激(rTMS)治疗焦虑症伴失眠的临床疗效。方法选取我院就诊的焦虑症伴失眠的患者58例,以随机数表法分为观察组和对照组各29例。观察组给予rTMS治疗,对照组口服文拉法辛+安定治疗。比较2组治疗前后汉密尔顿焦虑量表(HAMA)评分、多导睡眠监测睡眠潜伏期、觉醒次数及觉醒时间。结果治疗后观察组HAMA评分为(9.98±2.31)分,显著低于对照组的(15.26±3.03)分(P0.05);治疗前2组多导睡眠监测睡眠潜伏期、觉醒次数、觉醒时间比较均无明显差异(P0.05),治疗后观察组睡眠潜伏期(25.30±12.12)min、觉醒次数(3.11±2.01)次及觉醒时间(30.12±10.05)min均较对照组显著减少(P0.05)。结论 rTMS可显著改善伴失眠的焦虑症患者的症状,值得临床推广应用。     

右佐匹克隆联合米氮平对慢性失眠障碍的疗效分析

目的探讨右佐匹克隆联合米氮平对慢性失眠障碍患者的临床疗效。方法按随机数字法将82例慢性失眠患者分成研究组42例,对照组40例,对照组给予口服右佐匹克隆(1.5～3mg/d),研究组在对照组的基础上联合口服米氮平(15～30mg/d)治疗,在治疗前,治疗后1、2、4周分别对两组研究对象进行匹兹堡睡眠指数(PSQI)、不良反应量表(TESS)的评定;并以PSQI量表减分率进行有效率评定。同时在治疗前、治疗后4周对两组研究对象进行整夜睡眠呼吸监测(PSG),通过PSG睡眠指标观察对比两组治疗前后的变化。结果治疗后两组PSQI总分较治疗前均逐步下降,治疗4周后研究组有效率92.9%,对照组80%,差异具有统计学意义(χ2=11.296,P=0.010);研究组PSQI总分明显低于对照组,差异有统计学意义(P0. 05)。经治疗两组均出现TST延长,ATA、AT明显减少,SL明显缩短,SE明显提高,REM潜伏期缩短,REM、N2时间延长,与治疗前差异均有统计学意义(P0. 05);其中研究组对比治疗前还有N3时间及比例的明显增加,差异有统计学意义(P0. 05);治疗后研究组在TST、N2、N3时间及N3比例的增加,SL、ATA、AT的减少,SE的提高方面均较对照组明显,差异具有统计学意义(P0. 05)。结论右佐匹克隆联合米氮平对慢性失眠的治疗较单一使用右佐匹克隆疗效要好;安全性高,能加深睡眠,减少觉醒。     

失眠障碍患者小脑中央核磁共振波谱成像研究

目的研究未经药物治疗的失眠障碍患者小脑中央核氢质子磁共振波谱成像(proton magnetic resonance spectroscopy,~1H-MRS)特点。方法应用~1H-MRS技术检测23例未经药物治疗的失眠障碍患者(失眠组)和18名睡眠正常的对照者(对照组)小脑中央核N-乙酰天门冬氨酸(N-acetylaspartate,NAA)、胆碱复合物(choline-containing compounds,Cho)和肌酸(creatine,Cr)3种代谢物水平,并计算NAA/Cr和Cho/Cr比值。采用匹兹堡睡眠质量指数量表(Pittsburgh sleep quality index,PSQI)和失眠严重程度指数量表(insomnia severity index,ISI)评定所有受试者的主观睡眠质量和失眠严重程度;采用状态特质焦虑量表(state-trait anxiety inventory,STAI)和贝克抑郁量表(Beck depression inventory,BDI)评定受试者的焦虑、抑郁水平;采用多导睡眠图(polysomnography,PSG)测量客观睡眠参数。结果失眠组右侧小脑中央核NAA/Cr比值低于对照组(1.72±0.37 vs.2.03±0.50),差异有统计学意义(t=2.280,P=0.028)。对照组右侧小脑中央核NAA/Cr比值高于左侧(2.03±0.50 vs.1.68±0.21),差异有统计学意义(t=3.386,P=0.004),失眠组双侧小脑中央核之间NAA/Cr比值的差异无统计学意义(t=1.416,P=0.171)。所有受试者右侧小脑中央核NAA/Cr比值与PSQI总分呈统计学负相关(r=-0.369,P=0.018),与PSG入睡潜伏期(r=-0.437,P=0.004)、夜间觉醒次数(r=-0.432,P=0.005)分别呈统计学负相关,与3期睡眠比例呈统计学正相关(r=0.377,P=0.015)。结论失眠障碍患者小脑中央核NAA/Cr代谢存在右侧偏侧化紊乱,右侧小脑中央核可能存在神经元受损。     

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.     

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.     

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.     

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.     

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.