以蒙特卡洛方法建立组织中光剂量数学模型：分析激光对肝组织的损伤

背景：目前很难通过数学分析方法求出或临床直接监测激光能量在生物组织内的传输规律，因此常常采用数值模拟的方法进行预测。用蒙特卡罗方法研究激光光子在组织中的传输，是目前较为理想的研究方法。 目的：采用蒙特卡罗方法建立组织中的光剂量数学模型，探讨激光照射对于肝组织的损伤情况。 方法：采用蒙特卡罗方法，建立不同光学参数下正常组织和肿瘤组织的组织剂量数学模型，逐个计算大量光子迁移轨迹，统计嵌于正常组织和肿瘤组织中的光子宏观能量分布。 结果及结论：通过数学模型得到光损伤随组织深度的增加呈指数衰减的结果，且光子在组织边缘会形成第2个峰值。组织损伤是阈值过程，每条剂量曲线可被视为阈值曲线。采用蒙特卡罗方法模拟激光在肝组织中的传播，得到了激光光子在肝肿瘤组织中的分布规律。结果表明，适量光照强度能引起浅薄全面的肿瘤组织光损伤，深层光损伤伴随正常组织损伤。     

ZnPcS4-BSA对光动力杀伤胶质瘤细胞效应的影响及其机制研究

目的 研究新型光敏剂ZnPcS4-BSA对光动力杀伤人神经胶质瘤细胞U251效应的影响,并对机制进行初步探讨. 方法 紫外光谱法观察U251细胞对ZnPcS4-BSA的摄取规律,确定最佳孵育时间;CCK-8法测定不同浓度ZnPcS4-BSA、不同剂量激光辐射对U251的细胞毒性和ZnPcS4-BSA介导光动力疗法(PDT)的最佳浓度和最佳激光剂量;应用20 μmol/L ZnPcS4-BSA作用U251细胞4h后给予100 J/cm2的激光辐射,以同样条件培养而未作PDT治疗的细胞作为对照,流式细胞术、RT-PCR分别检测细胞凋亡率和VEGF基因表达的变化. 结果 紫外光谱法扫描发现ZnPcS4-BSA作用4h后U251细胞摄取ZnPcS4-BSA的量达到峰值.不同浓度ZnPcS4-BSA处理后细胞生存率的差异无统计学意义(P＞0.05).400J/cm2激光辐射后细胞生存率低于0、25、50、100、200J/cm2激光辐射组,差异有统计学意义(P＜0.05).30 μmol/L ZnPcS4-BSA作用U251细胞4h后给予25、50、100、200 J/cm2激光照射,随着激光剂量的增加,细胞存活率降低,差异有统计学意义(P＜0.05).20、40、60、80、100 μmol/L ZnPcS4-BSA作用U251细胞4h后,给予200J/cm2激光辐射,随着ZnPcS4-BSA浓度的增加,细胞的抑制率增加,差异有统计学意义(P＜0.05).与对照组比较,经20μmol/L ZnPcS4-BSA作用,100 J/cm2的激光辐射后U251细胞凋亡率、VEGF基因的表达升高,差异均有统计学意义(P＜0.05). 结论 新型光敏剂ZnPcS4-BSA具有良好的增强光动力效能,其介导的PDT能诱导细胞凋亡,其机制可能与VEGF基因有关.     

应用新型光敏剂ATX-S10.Na(Ⅱ)的光动力疗法治疗脑胶质瘤的实验研究

目的探讨在胶质瘤的光动力疗法中应用新型光敏剂ATX-S10.Na(Ⅱ)的可能性。方法首先对5种含有不同浓度的ATX-S10.Na(Ⅱ)的鼠和人的胶质瘤细胞中应用波长为670nm的激光照射,应用MTT法测定不同的肿瘤细胞对PDT治疗的反应。接着,在SD大鼠的C6胶质瘤皮下肿瘤模型应用中进行PDT治疗,探讨ATX-S10.Na(Ⅱ)介导的光化学反应所致的抗肿瘤作用。结果体外实验表明,PDT对肿瘤细胞的毒性作用既依靠ATX-S10.Na(Ⅱ)的药物浓度又依靠激光辐照的累计能量。每个细胞系的50%抑制浓度(IC50)波动于5-15μg/ml之间。在皮下肿瘤模型中,PDT治疗导致的肿瘤内部破坏面积随着激光能量的提高而增大,尤其是当照光剂量大于75J/cm时,与对照组相比有统计学意义。结论体外和在体的实验表明,新型光敏剂ATX-S10.Na(Ⅱ)介导的光动力疗法显示出极强的抗胶质瘤作用。     

垂体瘤的体外侵袭模型-Boyden小室法的建立和特点

目的　探讨Boyden小室体外侵袭模型适用于侵袭性垂体瘤研究的实验条件和方法。方法　选取手术切除的新鲜垂体瘤标本 5例,体外进行原代培养,肿瘤在影像学上均为一侧或双侧的颈内动脉被完全包绕或肿瘤破入蝶窦的侵袭性表现。将不同浓度 ( 0 5×105、1 0×105、1 5×105、2 0×105 /ml)的垂体瘤细胞 250μl置入Boyden小室侵袭模型,分别培养 (6、12、18、24)h,观察不同浓度细胞在不同时间穿透基质凝胶多孔滤膜的侵袭率。结果　在第 6h,透过基质凝胶多孔滤膜的细胞还很少,随时间的延长而增多,在 12h前后增幅最明显, 18h以后有逐渐饱和的趋势;同时,随细胞浓度的增高,透过细胞比率也增加,但细胞浓度大于 1 0×105 /ml时,瘤细胞的侵袭百分率变化不显著。结论　Boyden小室侵袭模型适用于原代培养垂体瘤细胞的条件是,在 1 0×105 /ml细胞浓度下培养12h后,计算细胞的侵袭率。     

5-氨基乙酰丙酸介导的光动力对人脑胶质瘤细胞的治疗作用

目的探讨5-氨基乙酰丙酸(5-ALA)介导的光动力学对人脑胶质瘤U251细胞的治疗作用方法使用荧光显微镜及共聚焦显微镜检测5-ALA所产生的光敏剂原卟啉(PpIX)在U251细胞中的定位。将5-ALA加入U251细胞中,随之以635nm的激光辐射,使用MTT法测定细胞生存率结果5-ALA与U251细胞共培养可以产生光敏剂原卟啉。原卟啉弥散地分布在U251细胞的胞浆中,胞核区未见分布。5-ALA介导的光动力对人脑胶质瘤U251细胞的杀伤作用随着5-ALA与U251细胞孵育时间的延长及5-ALA浓度的增加而增加,但在孵育6h、5-ALA浓度为2mmol/L时达饱和。而单用5-ALA或单纯激光辐射,对U251细胞无明显的杀伤作用。结论5-ALA介导的光动力治疗是很有前途的人脑胶质瘤治疗方法,5-ALA与U251细胞孵育的最佳时间为6h,最佳5-ALA药物浓度为2mmol/L     

骨髓间充质干细胞对系统性红斑狼疮患者T细胞活化的影响

背景：骨髓间充质干细胞具有免疫调节作用,可治疗自身免疫性疾病。 目的：探讨在体外人骨髓间充质干细胞对系统性红斑狼疮患者T细胞活化的影响。 方法：分离、培养人骨髓间充质干细胞,培养至第3代以后的细胞胰蛋白酶消化后用流式细胞仪确定其浓度,按照不同浓度将骨髓间充质干细胞设为1×108,1×107L-1两组。取肝素抗凝新鲜27例系统性红斑狼疮患者患者外周血10 mL,分离培养T淋巴细胞,以1×109 L-1的细胞浓度,100 µL/孔,接种两组骨髓间充质干细胞上,以单纯统性红斑狼疮患者的T淋巴细胞作为对照组。通过流式细胞术计算CD3+ T细胞CD25(IL-2R)和CD38细胞的表达率。 结果与结论：与对照组比较,1×108 L-1浓度组的骨髓间充质干细胞对系统性红斑狼疮患者CD25及CD38的表达呈明显抑制作用(P < 0.01),1×107 L-1浓度组,无明显变化。结果表明：骨髓间充质干细胞抑制系统性红斑狼疮患者T细胞的活化,且对这种抑制作用具有数量依赖性。     

海藻酸钠-多聚赖氨酸-海藻酸钠微囊内细胞浓度与胰岛素和C肽的释放**

摘要 背景：微囊化已经普遍应用于各种实验研究,微囊包裹的干细胞治疗糖尿病问题也成为当今的热点,但是囊内包裹的细胞浓度与胰岛素释放量的关系成为目前需要解决的问题之一。 目的：运用海藻酸钠-多聚赖氨酸-海藻酸钠微囊包裹胰岛素产生细胞,观察细胞浓度对胰岛素和C肽释放情况的影响。 方法：制备大鼠胰腺损伤提取物,将小鼠骨髓间充质干细胞诱导分化为胰岛素产生细胞。免疫荧光和双硫腙染色鉴定诱导后细胞内胰岛素的表达。然后将胰岛素产生细胞制成浓度分别为1×107 L-1,5×107 L-1,1×108 L-1,5×108 L-1,1×109 L-1,5× 109 L-1的细胞悬液,气体吹喷法制成微囊,用6-羧基乙二酸荧光素检测囊内细胞活力,用葡萄糖刺激微囊内细胞检查其胰岛素和C肽的分泌情况。 结果与结论：胰腺损伤提取物诱导后双硫腙染色和细胞免疫荧光鉴定出胰岛素产生细胞内有胰岛素的表达;胰岛素产生细胞制成的微囊直径约为400 µm,大小均一,6-羧基乙二酸荧光素检测到囊内细胞的活力很好。用葡萄糖刺激不同细胞浓度的微囊,发现细胞浓度为1×108 L-1时,胰岛素和C肽的分泌达到最高。 关键词：微囊化;骨髓间充质干细胞;胰岛素产生细胞;胰岛素;C肽 doi:10.3969/j.issn.1673-8225.2011.03.046     

人脂肪神经干细胞移植对大鼠脑缺血后血管新生和细胞因子的作用

背景：近年来研究发现，骨髓造血微环境尤其是骨髓间充质干细胞在白血病细胞恶性克隆的增殖、分化和凋亡中发挥重要作用。 目的：探讨联合正常人骨髓间充质干细胞共培养后，K562细胞的增殖情况及对化疗敏感性的变化。 设计、时间及地点：细胞学体外对照观察，于2007-06/2008-06在南京医科大学附属南京儿童医院完成。 材料：骨髓来源于南京医科大学附属南京儿童医院骨科收治的下肢骨折需手术的患儿。 方法：percoll密度梯度离心法分离培养人骨髓间充质干细胞。设立2组：单独培养组培养皿中只接种处于对数生长期的K562细胞1×106个；共培养组培养皿中按2×108 L-1接种第3代人骨髓间充质干细胞，3 d后全量换液，再加入处于对数生长期的K562细胞1×106个，共培养24 h。消化收集两组K562细胞，分别加入质量浓度为0.1，0.2，0.4，0.8 mg/L的阿糖胞苷，再次培养24 h。 主要观察指标：骨髓间充质干细胞对K562细胞生长曲线、细胞周期的影响。不同质量浓度阿糖胞苷干预后K562细胞凋亡率的变化。 结果：与单独培养组比较，共培养组K562细胞数明显降低，至第7天仅为单独培养组的57.7%；G0/G1期、G2期共培养组K562细胞比例明显增加（P均< 0.05），S期、S+G2期共培养组K562细胞比例显著减少（P < 0.01，P < 0.05）。阿糖胞苷质量浓度为0.1~0.8 mg/L时，对K562细胞诱发凋亡作用逐渐增强；在相同质量浓度的阿糖胞苷干预下，共培养组K562细胞凋亡率明显低于单独培养组（P < 0.05）。 结论：与骨髓间充质干细胞共培养后，K562细胞的生长受到抑制，且处于增殖期的细胞比例下降，主要阻滞于G0/G1期。骨髓间充质干细胞对K562细胞具有保护作用，可降低阿糖胞苷诱导K562细胞的凋亡率，产生化疗耐药。     

骨髓间充质干细胞对K562细胞增殖及化疗敏感性的影响

背景：近年来研究发现，骨髓造血微环境尤其是骨髓间充质干细胞在白血病细胞恶性克隆的增殖、分化和凋亡中发挥重要作用。 目的：探讨联合正常人骨髓间充质干细胞共培养后，K562细胞的增殖情况及对化疗敏感性的变化。 设计、时间及地点：细胞学体外对照观察，于2007-06/2008-06在南京医科大学附属南京儿童医院完成。 材料：骨髓来源于南京医科大学附属南京儿童医院骨科收治的下肢骨折需手术的患儿。 方法：percoll密度梯度离心法分离培养人骨髓间充质干细胞。设立2组：单独培养组培养皿中只接种处于对数生长期的K562细胞1×106个；共培养组培养皿中按2×108 L-1接种第3代人骨髓间充质干细胞，3 d后全量换液，再加入处于对数生长期的K562细胞1×106个，共培养24 h。消化收集两组K562细胞，分别加入质量浓度为0.1，0.2，0.4，0.8 mg/L的阿糖胞苷，再次培养24 h。 主要观察指标：骨髓间充质干细胞对K562细胞生长曲线、细胞周期的影响。不同质量浓度阿糖胞苷干预后K562细胞凋亡率的变化。 结果：与单独培养组比较，共培养组K562细胞数明显降低，至第7天仅为单独培养组的57.7%；G0/G1期、G2期共培养组K562细胞比例明显增加（P均< 0.05），S期、S+G2期共培养组K562细胞比例显著减少（P < 0.01，P < 0.05）。阿糖胞苷质量浓度为0.1~0.8 mg/L时，对K562细胞诱发凋亡作用逐渐增强；在相同质量浓度的阿糖胞苷干预下，共培养组K562细胞凋亡率明显低于单独培养组（P < 0.05）。 结论：与骨髓间充质干细胞共培养后，K562细胞的生长受到抑制，且处于增殖期的细胞比例下降，主要阻滞于G0/G1期。骨髓间充质干细胞对K562细胞具有保护作用，可降低阿糖胞苷诱导K562细胞的凋亡率，产生化疗耐药。     

嗅鞘细胞与神经干细胞共培养后增殖及向神经元的分化

背景：影响神经干细胞增殖分化的外在因素包括细胞因子和微环境,嗅鞘细胞能分泌多种细胞因子,与神经干细胞共培养时改变其微环境。 目的：观察不同浓度嗅鞘细胞对神经干细胞增殖及分化的影响。 方法：体外分别培养Wistar大鼠神经干细胞和嗅鞘细胞,5×107 L-1神经干细胞分别和1×107 L-1,1×109 L-1,1×1011 L-1嗅鞘细胞共培养,同时设立正常对照组,不加嗅鞘细胞。倒置荧光显微镜下观察神经干细胞增殖情况,诱导7 d后行NSE免疫细胞化学染色,计算阳性细胞/细胞总数得出阳性细胞百分比。 结果与结论：①3种浓度嗅鞘细胞与神经干细胞共培养3 d后,均促进了神经干细胞增殖,以1×109 L-1嗅鞘细胞共培养组作用最显著,明显优于1×107 L-1嗅鞘细胞组、1×1011 L-1嗅鞘细胞组。②神经干细胞与1×109 L-1嗅鞘细胞共培养7 d后,神经干细胞分化为神经元样细胞的百分比最高,与正常对照组相比差异有显著性意义(P < 0.01)。     

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.