阿尔茨海默病患者服用达纳康前后血浆4种神经肽的动态变化

目的　观察早期阿尔茨海默病 (AD)患者服用达纳康 (系法国银杏叶制剂 )治疗前后血浆生长抑素 (somatostatin ,SS)、精氨酸加压素 (argininevasopressin,AVP)、促肾上腺皮质激素 (corticotropin ,ACTH)及β内啡肽 (β endorphin ,β EP) 4种神经肽含量的影响。 方法　对 2 7例早期AD患者于达纳康治疗前后分别取血浆测定上述 4种神经肽含量 ,同时作简易智力状态检查 (MMSE)和韦氏成人智力量表 (中国修订 )(WAIS RC)测评 ,并与 30例正常老年人作对照。结果　AD组血浆AVP含量 (35.8± 1 9.2 4 )ng/L较对照组 (56.3± 2 0 .8)ng/L显著减少 (P <0 0 5) ;血浆SS、ACTH含量在治疗前分别为 (348.8± 2 1 0 .3)ng/L和 (8.2 5± 3 .85)ng/L ,治疗后则分别上升为 (881 .4± 363 .1 6)ng/L和 (1 9± 9.1 1 )ng/L。治疗前后比较均有非常显著性差异 (P <0 .0 0 1 )。AVP在治疗后血浆含量也有升高为 (57.85± 1 6 .86)ng/L,与治疗前比较有显著性差异(P <0 .0 5)。结论　早期AD患者血浆AVP含量减少 ,提示AVP可作为AD患者早期生化指标。早期AD患者在服用达纳康后SS、ACTH、AVP血浆含量均显著上升 ,提示SS、ACTH、AVP可能参与AD的发病机制     

精神分裂症患者氯氮平治疗前后免疫指标的变化

目的　探讨精神分裂症患者抗精神病药物氯氮平治疗前后总T细胞 (CD3 )、T辅助 /T诱导细胞 (CD4)、T抑制 /T杀伤细胞 (CD8)及血清白细胞介素 6 (IL 6 )水平的变化。方法　对 6 6例精神分裂症患者 (男 32例 ,女 34例 )和 30名健康对照者 (男 16名 ,女性 14名 )的血清CD3 、CD4、CD8、CD4/CD8及IL 6的水平进行检测。用酶联免疫吸附法 (ELISA)及碱性磷酸酶抗碱性磷酸酶法 (APAAP)检测各受试者血清IL 6及T细胞亚群。结果　 (1) 6 6例精神分裂症患者治疗前CD3 、CD4、CD8、CD4/CD8比值均低于对照组 (P <0 0 1～ 0 0 0 1) ,而IL 6 [(1 8± 0 6 )ng/L]则高于对照组 [(1 2± 0 6 )ng/L],P <0 0 0 1;(2 )氯氮平治疗后CD3 、CD4、CD4/CD8高于治疗前 (P <0 0 1) ;(3)阳性、阴性组患者治疗前CD3 、CD4、CD8、CD4/CD8均低于对照组 (P <0 0 1) ,而IL 6水平则高于对照组高 (P <0 0 1) ;(4)治疗后阳性、阴性组患者IL 6水平 [(1 2± 0 3)ng/L、(1 1± 0 5 )ng/L]均较治疗前有所降低 ,与对照组的差异无显著性 (P >0 0 5 ) ;(5 )阳性、阴性组患者治疗后组间比较 ,阳性组CD3 、CD4、CD4/CD8明显高于阴性组 ,CD8低于阴性组 (P <0 0 5 ) ,两组间IL 6水平的差异无显著性 (P >0 0 5 ) ;(6 )多元逐步回归分析显示 ,阳     

首发精神分裂症患者氯氮平治疗前后血浆白细胞介素6,13及可溶性白细胞介素6受体水平的变化

目的探讨首发精神分裂症患者氯氮平治疗前后血浆白细胞介素6(IL6)、白细胞介素13(IL13)及可溶性白细胞介素6受体(sIL6R)水平的变化。方法采用双抗体夹心ABC放射免疫吸附法,对30例(男10例,女20例)首发精神分裂症患者(患者组)氯氮平治疗前后及28名(男13名,女15名)健康对照者(对照组)的血浆IL6、IL13及sIL6R水平进行检测。结果(1)患者组治疗前[(202±26)ng/L]后[(217±28)ng/L]血浆IL6水平均明显高于对照组[(181±36)ng/L],差异均有统计学意义(均P<005)。患者组氯氮平治疗后血浆IL6水平高于治疗前(P<005)。(2)患者组治疗第6周末血浆sIL6R水平[(23±20)ng/L]比治疗前[(34±16)ng/L]明显下降,差异有统计学意义(P<005)。(3)患者组治疗前血浆IL13水平[(16±12)ng/L]明显低于对照组[(24±18)ng/L],差异有统计学意义(P<005),治疗第6周末[(22±14)ng/L]比治疗前有所升高。(4)经相关及多元回归分析,患者组治疗第6周末血浆IL6水平的增高幅度与氯氮平治疗剂量呈正相关,差异有统计学意义(r=0722,P=0000);治疗前血浆sIL6R水平与阳性症状分呈正相关(r=0379,P=0020),血浆IL13水平与阴性症状分(r=-0602,P=0000)及阳性和阴性症状量表总分(r=-0334,P=0035)呈负相关;治疗前后IL13的变化幅度与阴性症状分减分率呈正相关(r=0611     

白细胞介素-2及其受体在癫痫患者发作中的变化和对癫痫大鼠的致惊作用

目的探讨白细胞介素-2(interluekin-2, IL-2)及其可溶性受体在癫痫患者发作中的变化和对癫痫大鼠的致惊作用.方法采用ELISA方法检测58例癫痫患儿和23例健康儿血清IL-2及其可溶性受体的浓度,并进行分组比较;观察侧脑室注射IL-2对遗传性癫痫易感大鼠(P77PMC)惊厥发作的影响.结果癫痫组血清IL-2及其可溶性受体浓度[(25.86±5.21) ng/mL和(758.26±78.49) U/mL ]明显高于对照组[(13.78±3.24) ng/mL和(325.67±34.58) U/mL](P<0.01),且发作期[(30.31±6.77) ng/mL和(806.25±112.35) U/mL]高于间歇期[(20.27±4.66) ng/mL和(584.15±57.85) U/mL ](P<0.01),脑电图异常者[(27.18±4.35) ng/mL和(724.48±78.56) U/mL]高于正常者[(20.04±3.55) ng/mL和(621.85±77.45) U/mL],但与发作类型、病程长短及经治疗与否无关;侧脑室注射IL-2(5 000 U/L)5～10 μL后大鼠惊厥评分从26升高到36(P<0.05),惊厥持续时间从32 s延长到65 s(P<0.01),但对潜伏期无影响.结论 IL-2在癫痫患者处于高水平状态,直接侧脑室注射IL-2可加重大鼠惊厥程度,提示其参与癫痫发病过程.     

强迫症、抑郁症及焦虑症患者血小板5-羟色胺浓度的对照研究

目的　研究 5 羟色胺 ( 5 HT)在强迫症发病中的作用及强迫思维与强迫动作亚组、抑郁症及焦虑症患者间血小板 5 HT含量的差异。方法　采用高效液相色谱法 ,分别测定 2 9例强迫症患者 [(强迫症组 ,根据Y BOCS强迫量表因子得分将其分为强迫思维 ( 16例 )、强迫动作 ( 7例 )和混合性( 6例 ) 3组 ]、2 0例抑郁障碍患者 (抑郁症组 )、17例焦虑障碍患者 (焦虑症组 )和 2 8名正常人 (正常人组 )的血小板 5 HT含量。结果　强迫症组血小板 5 HT水平 [( 139± 172 ) μg/L]低于正常人组 [( 2 4 8±2 15 ) μg/L]及焦虑症组 [( 397± 4 0 1) μg/L],差异具有显著性 (P =0 0 39;P =0 0 2 0 ) ;与抑郁症组 [( 2 0 2± 16 2 ) μg/L]的差异无显著性 ( P >0 0 5 ) ;强迫思维 [( 85± 6 6 ) μg/L]与强迫动作组 [( 16 9± 10 0 ) μg/L]间血小板 5 HT含量的差异有显著性 (P =0 0 2 5 )。结论　强迫症患者 5 HT浓度变化与抑郁障碍患者趋同 ,与焦虑障碍患者的差异有显著性 ;单纯强迫思维者的 5 HT浓度与单纯强迫动作患者的差异有显著性     

重性抑郁症患者脑脊液中P物质、神经肽Y、5-羟色胺及去甲肾上腺素含量的研究

目的从神经递质角度探讨重性抑郁症的病理生理机制。方法采用酶联免疫吸附法测定40例重性抑郁症患者(患者组)、40例对照(前列腺增生症、鞘膜积液、腹股沟疝患者及部分健康人,对照组)脑脊液中P物质(SP)、神经肽Y(NPY)、去甲肾上腺素(NE)、5-羟色胺(5-HT)及5-羟吲哚乙酸含量。结果患者组SP含量[(18±24)ng/L]高于对照组[(9±13)ng/L],差异有统计学意义(P=0.010)。患者组NE[(92±88)ng/L]高于对照组[(51±35)ng/L],差异有统计学意义(P=0.009)。患者组5-HT含量女性[(0.59±0.13)μg/L]低于男性[(0.82±0.32)μg/L],差异有统计学意义(P=0.014)。患者组有自杀行为和强烈自杀观念患者的5-HT含量低于无自杀观念患者,差异有统计学意义(P分别为0.018和0.023);有自杀行为患者的NE含量高于无自杀观念和偶有自杀观念患者,差异有统计学意义(P分别为0.029和0.017)。复发性抑郁症的NPY含量[(152±89)ng/L]明显高于首发性抑郁症[(83±32)ng/L],P=0.026。5个测定指标含量间无明显相关关系。结论重性抑郁症患者可能存在多种神经递质功能异常。     

颈动脉粥样硬化斑块及相关生化指标与脑梗死的关系

目的　探讨颈动脉粥样硬化斑块及其相关生化指标与脑梗死的关系。方法　对 6 5例脑梗死患者 (脑梗死组 )及 35例非脑梗死患者 (对照组 )分别进行彩色多普勒超声检测 ,并记录两组颈动脉粥样硬化斑块的部位、数目、性质和颈动脉内径 ;同时检测两组的血脂、血糖和纤维蛋白原等生化指标。结果　脑梗死组颈动脉粥样硬化斑块检出率、左右颈总动脉内径 [81 5 4 %、(7 4 3± 0 0 7)mm、(7 5 2± 0 6 0 )mm]与对照组[2 8 5 7%、(7 75± 0 10 )mm、(7 97± 0 75 )mm]比较差异均有显著性 (均P <0 0 5 )。粥样硬化斑块位于颈总动脉最多 (78 2 3% ) ,其次是颈总动脉分叉处 (14 5 2 % ) ,颈内动脉颅外段最少 (7 2 5 % )。斑块部位与脑梗死部位有显著同侧相关性 (P <0 0 5 ) ;脑梗死组三酰甘油 (TG) [(1 81± 0 12 )mmol/L]、餐后 2h血糖 [(9 2 2± 0 4 3)mmol/L]及纤维蛋白原 [(3 18± 0 0 7)mmol/L]也均显著高于对照组 [(1 39± 0 0 9)mmol/L、(8 2 0± 0 35 )mmol/L、(2 6 4± 0 14 )mmol/L](均P <0 0 5 ) ;脑梗死组中颈总动脉内径与TG有显著正相关性 (r=0 34,P <0 0 1) ,与高密度脂蛋白 (HDL)存在显著负相关 (r=- 0 2 5 ,P <0 0 5 )。结论　颈动脉粥样硬化斑块与脑梗死发生有密切关系 ,部分脂质     

利培酮对精神分裂症患者血浆高香草酸的影响

目的　探讨利培酮对精神分裂症患者中枢多巴胺代谢产物血浆高香草酸 (pHVA)的影响。方法　 30例精神分裂症住院患者 (患者组 )纳入研究 ,利培酮治疗平均剂量为 (3 2± 1 1)mg/d ,共观察 6周。以阳性和阴性症状量表 (PANSS)评定疗效 ,以高效液相库仑阵列电化学检测法测定患者治疗前后的 pHVA含量。 30例健康志愿者作为对照组 ,检测pHVA水平。 结果　 (1)患者组治疗前 pHVA含量 [(7 9± 4 0 ) μg /L]与对照组含量 [(8 8± 4 1) μg /L]的差异无显著性 (P >0 0 5 ) ,而患者组治疗后 pHVA含量 [(5 3± 2 7) μg/L]明显低于治疗前 (P <0 0 1) ;(2 )治疗前患者组 pHVA与PANSS阳性症状评分 [(2 0 7± 4 1)分 ]存在正相关 (r =0 39,P <0 0 0 1) ,与基线PANSS阴性症状评分 [(19 7± 5 1)分 ]存在负相关 (r =- 0 35 ,P <0 0 1) ;(3)基础pHVA含量及其治疗前后差值[(2 6± 1 3) μg/L]与PANSS阳性症状评分减分值 [(10 8± 4 1)分 ]均分别呈正相关 (r =0 4 8,P <0 0 1;r=0 6 0 ,P <0 0 0 1)。结论　患者组治疗前pHVA可部分反映精神分裂症症状 (尤其是阳性症状 )的严重程度 ,基础 pHVA含量及治疗前后pHVA水平的变化与利培酮治疗阳性症状的疗效相关。     

首发精神分裂症患者白细胞介素4,10,12及干扰素-γ水平与相关因素研究

目的研究首发精神分裂症患者血清白细胞介素(IL)4、IL-10、IL-12及干扰素-γ(IFN-γ)水平与病程及精神症状严重程度的相关性.方法患者组为30例符合入组标准的首发精神分裂症患者,对照组为58名符合入组标准的正常人.应用夹心酶联免疫吸附测定法测定血清中IL-4,IL-10,IL-12及IFN-γ浓度水平.应用简明精神病评定量表、阳性和阴性症状量表对患者进行精神症状评定.结果患者组IL-4[ (68±29) ng/L]、IL-10为[(61±25) ng/L]均明显高于对照组 [(50±23) ng/L,(32±18) ng/L],差异有非常显著性(P=0.01,P=0.00);IL-12 [(35±15) ng/L]明显低于对照组[(53±27) ng/L],差异有显著性(P=0.01); IFN-γ [(41±17) ng/L]与对照组 [(51±23) ng/L]的差异无显著性(P=0.09).首发精神分裂症患者血清IL-4、IL-10、IL-12及IFN-γ浓度水平与病程无相关(r=0.09,0.07,-0.20,-0.21;P=0.63,0.71,0.30 , 0.27), IL-4、IL-10、IL-12及IFN-γ浓度水平均与精神症状评定无显著相关(P＞0.05).患者组IL-4 浓度水平与IL-10的浓度水平正相关(r=0.52,P=0.03),IL-12与IFN-γ浓度水平也存在正相关关系(r=1.00,P=0.00).对照组4种细胞因子间均无相关(P＞0.05).结论首发精神分裂症患者IL-4、IL-10、IL-12及IFN-γ浓度水平存在紊乱,但与精神症状严重程度及病程长短无相关性.     

广泛性焦虑症与抑郁症患者免疫、内分泌及单胺递质的对照研究

目的探讨广泛性焦虑症(GAD)与抑郁症(MD)患者在免疫、内分泌和单胺递质方面的差异。方法 对30例GAD患者(焦虑症组)、38例MD患者(抑郁症组)在治疗(5-羟色胺再摄取抑制剂治疗6~8周)前后分别检测血清白细胞介素2(IL-2)、白细胞介素6(IL-6)、白细胞介素1β(IL-1β)、白细胞介素8(IL-8)、可溶性白细胞介素6受体(SIL-6R)、肿瘤坏死因子α(TNF-α)、皮质醇(CS)、促肾上腺皮质激素(ACTH)、肾上腺素(EPH)和去甲肾上腺素(NE)水平。选择30名年龄和性别与患者组相匹配的健康人为对照组。结果 (1)焦虑症组治疗前IL-8[(122±76)ng／L]、SIL-6R[(2 065±790)ng／L]水平均高于对照组(99±68)ng／L]、[(294±48)ng／L,IL-6水平为(1.6±0.7)ng／L,低于对照组[(5.3±2.7)ng／L],差异均有显著性意义(P<0.05);抑郁症组治疗前IL-2[(7.7±6.7)ng／L]、IL-8[(119±67)ng／L]、SIL-6R[(1308±371)ng／L]水平均高于对照组,差异均有显著性意义(均P<0.05)。经治疗后,焦虑症组IL-6[(4.3±1.2)ng／L]水平较治疗前升高,IL-8[(39±9)ng／L]水平较治疗前降低(P<0.05);抑郁症组IL-2[(2.4±1.2)ng／L]、IL-8[(47±15)ng／L]水平较治疗前降低(P<0.05);均接近于对照组水平(均P>0.05)。(2)焦虑症组治疗前ACIH[(49±28)ng／L]、EPH[(67±45)ng／     

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.     

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.     

Pediatric Epilepsy Surgery

Summary: The use of implantable arrays of epidural electrodes has made it possible to carry out extraoperative electrocorticography (ECoG) and functional localization in the awake child. This has permitted cortical excisions that are determined by criteria similar to those obtained during surgical procedures performed under local anesthesia in adults. In addition, the method also permits simultaneous ECoG and video monitoring during the child's symptomatic seizures, providing additional important localizing information that is impractical to obtain in operations under local anesthesia. We report our experience with 75 children, ages 5 months to 15 years, whom we have managed with epidural electrode arrays. The method of extraoperative ECoG is described and illustrative cases are presented to demonstrate its feasibility and utility in children. In addition, we call attention to gliomas as a common cause of chronic focal seizures in children. Of 49 children undergoing resection and followed for from 1 to 14 years (mean of 5.8 years), 32 (65%) are either seizure free or have had a significant reduction in seizure frequency that has unambiguously improved their quality of life. The results are analyzed further by relating the surgical outcome to each of the pathologic entities that caused the seizures. This analysis reveals the variety of neurological conditions that commonly cause intractable focal seizure disorder in children and distinguishes those pathologic entities in which the seizure disorder is apt to respond to surgical intervention from those that will not.     

Un nouveau cadre conceptuel de travail pour une psychiatrie revisitée ? Introduction à deux articles de E. Kandel

In two articles which appeared in the American Journal of Psychiatry and that were subsequently translated for Évolution Psychiatrique, E. Kandel examines the bases for a reinterpreted psychiatry that is prepared to confront the major challenge of the 3rd millenium: that of insight into the mind and brain. This requires a major reorganization of the discipline, which involves a reinvestment of the scientific approach and a critical  assessment of the data provided by psychoanalytical psychiatry and cognitive neurosciences. Seven concepts have therefore been proposed for interactive re-examination: consciousness, the unconscious, memory, emotion, development, desire, impulse. The dynamic relations existing between genetics and the environment allow one to see how evolutions are possible from actions at different levels, both psychotherapeutic and pharmacological. Imaging and other techniques provide additional objective information to the process of human interaction which remains the basis of psychiatry. A common framework for psychiatry and the neurosciences, a reconsideration and renewal of the psychoanalytical approach are both possible and necessary.     

Opioids and the developing organism: A comprehensive bibliography, 1984–1988

A comprehensive bibliography of the literature concerned with opioids and the developing organism for 1984-1988 is presented. Utilized with companion papers (Neurosci. Biobehav. Rev. 6:439-479; 1982; 8:387-403; 1984), these articles cover the clinical and laboratory references beginning in 1875. For the years 1984, 1985, 1986, 1987, and 1988, a total of 877 citations were recorded. A series of indexes accompanies the citations in order to make the literature more accessible. These indexes are divided into clinical and laboratory topics, and subdivided into such topics as the type of opioid explored and the general area of biological interest (e.g., physiology).     

La biologie et le futur de la psychanalyse : un nouveau cadre conceptuel de travail pour une psychiatrie revisitée

The American Journal of Psychiatry has received a number of letters in response to my earlier “Framework” article (1). Some of these are reprinted elsewhere in this issue, and I have answered them briefly there. However, one issue raised by some letters deserves a more detailed answer, and that relates to whether biology is at all relevant to psychoanalysis. To my mind, this issue is so central to the future of psychoanalysis that it cannot be addressed with a brief comment. I therefore have written this article in an attempt to outline the importance of biology for the future of psychoanalysis.     

Facteurs de risque environnementaux à la schizophrénie

Schizophrenia is currently a major concern, its prevalence being estimated at around 1% and its social consequences being severe. The elucidation of the pathophysiology of the disease is difficult due to the great variability of clinical expressions, the instability of the clinical symptoms during the evolution and the absence of reliable biological markers. The existence of a familial aggregation in schizophrenia is well known, the risk of presenting the disease for first-degree relatives of patients being 5 to 10 times higher than the risk observed in the general population. The genetic component was further confirmed by twin and adoption studies. Although the concordance for the disease is higher (40 to 70%) among monozygotic twins as compared with dizygotic twins (15%) it does not reach 100%, which implies that environmental factors modulate the effects of the genotype. However, the role of these factors and especially their interaction with genetic factors remain unclear but the implications of some specific environmental factors are well documented by recent research data. The current literature on sex differences in schizophrenia is consistent. Several studies have suggested that male and female patients may differ in age at the onset and expression of clinical symptoms. Complications during pregnancy or birth-giving may increase the risk of developing schizophrenia later in life. The major complications are oxygen deprivation during pregnancy, bleeding, maternal malnutrition or infection (exposure to influenza, for example). A low birth weight is associated with an increased risk of schizophrenia. Psychoses are more common among people living in an urban environment and among those born during winter months. Schizophrenia is probably more prevalent in people who are living promiscuously, are subject to toxic abuse, poor nutrition and stress but here more precise data are needed. Moreover, immigrants have a higher risk of developing psychotic disorders. In addition, head traumas are associated with an increased risk of schizophrenia. Though they are contentious, some studies suggest that substance abuse (cannabis use in European countries) is related to the development of schizophrenia, especially in people with genetic vulnerability. Moreover, substance misuse may worsen the symptoms. If the environment is sufficiently stressful, people with a high genetic vulnerability will develop some degree of mental illness, including schizophrenia. Conversely, a less stressful or a protective environment may decrease the risk of its onset in persons with a predisposition to schizophrenia.     

Introduction: Goals

Summary: Epilepsy is characterized by recurrent seizures. Many epilepsies with focal seizures as well as convulsive generalized seizures respond satisfactorily to antiepileptic drugs (AEDs) that reduce repetitive firing (e.g., phenytoin, carbamazepine, and valproate) or that augment GABA_A-mediated inhibition (e.g., phenobarbital and benzodiazepines). A number of drugs presently under development, such as NMDA receptor antagonists, loreclezole, losigamone, meth-ysticine, and dextromethorphan, are promising in acute animal models of otherwise drug-resistant convulsant activity. As a result of recent studies in both experimental models and surgically resected human epileptic brain, the prospects for development of AEDs have significantly improved. Several new AEDs recently have reached the commercial market or are in experimental or clinical trials. A comparative presentation of the standing of the new AEDs with respect to their efficacy and side effects is necessary, but still very difficult. Because initial experience with new AEDs is restricted to populations with severe drug-resistant epilepsy, the crucial question whether potential new AEDs can alter prognosis is not yet definitively answered. There is a clear need to compare the effects of standard AEDs and new AEDs in naive patients and over longer follow-up periods. Moreover, because of the strong desire to develop antiepileptic therapy that directly treats the primary etiology of a given epileptic syndrome , or modifies the neurobiological processes that cause recurrent seizures, better experimental epilepsy models for chronic epilepsy and further clinical studies are necessary to increase the knowledge on the pathophysiology of distinct epileptic syndromes. In this respect, studies on the differences between responders and nonresponders to a given AED treatment are extremely valuable.