抑郁症患者脑电超慢涨落检测分析

目的:探讨抑郁症患者脑内神经递质活动变化。方法:应用中国北京ML2001脑电超慢涨落分析仪,通过对14例抑郁症患者于治疗前及治疗2、4周后脑电超慢涨落图(EFG),分析其谱线变化来反映脑内神经递质活动变化。结果:14例抑郁症患者治疗前脑内神经递质值与正常值对照比较,其5羟色胺(5HT)、乙酰胆碱(ACh)、去甲肾上腺素(NE)、多巴胺(DA)均降低,但以ACh、DA差异有显著性。治疗前及抗抑郁药治疗2、4周EFG值比较,其γ氨基丁酸(GABA)、谷氨酸(Glu)明显降低,而5HT、ACh、DA显著升高,差异有显著性。结论:脑内神经递质GABA、Glu、5HT、ACh、NE、DA间的协同不良可能导致了抑郁症发作,抗抑郁药治疗后脑内神经递质变化较大,单胺类递质活性增强。     

28h睡眠剥夺对脑内神经递质和脑功能的影响

目的 探索28 h睡眠剥夺对脑内神经递质的变化及脑功能的影响.方法 对9例健康被试在28 h睡眠剥夺前后进行脑电超慢涨落图检查,分析其在睡眠剥夺前后神经递质及脑功能的动态变化情况.结果 (1)被试在睡眠剥夺后脑内各种神经递质均有所变化,其中Glu、Ach和NE活动显著性减弱,GABA活动显著性增强,P均＜0.05;(2)被试在SD前后熵值均有一定的变化,其中O1和O2电极处在SD后熵值显著性增高,P均＜0.05;(3)被试缺血缺氧,疲劳状态程度在SD后均有加重.结论 脑电超慢涨落技术通过检测个体在28h睡眠剥夺前后的神经递质的动态变化,可以为脑力疲劳提供客观依据.     

抑郁症患者中枢神经递质活动的脑电超慢涨落图分析

目的探讨抑郁症患者的脑电超慢涨落图(Encephalofluctuograph,EFG)的特征。方法对符合《中国精神障碍与诊断标准(第3版)》(CCMD-3)抑郁症诊断标准的51例门诊及住院抑郁症患者,采用EFG分析仪检测其中枢神经递质活动变化情况及其脑功能状态,与正常对照组进行比较。结果抑郁症患者中枢神经递质γ-氨基丁酸(GABA)、谷氨酸(Glu)、5-羟色胺(5-HT)、乙酰胆碱(Ach)、去甲肾上腺素(NE)及多巴胺(DA)等功率的实测值都低于正常对照组,差异均有统计学意义(P均0.05)。相对功率5-HT明显升高而DA的相对功率明显下降(P0.05)。脑功能状态指数中的运动指数下降,差异有统计学意义(P0.05),而兴奋抑制指数和血管舒缩指数的实测值差异无统计学意义(P0.05)。结论抑郁症患者脑内主要神经递质功率均明显降低,其脑功能状态存在不同程度的异常。     

首发精神分裂症患者脑电超慢涨落图分析

目的探讨脑电超慢涨落图（ET）与阴性、阳性精神分裂症异质性的关系。方法对首次发作未用药精神分裂症患者50例进行阳性阴性临床症状量表（PANSS）评定和脑电超慢涨落图检测。结果阴性、阳性精神分裂症组与正常对照组相比，NE、5-HT活动显著降低，DA活动显著升高，差异具有统计学意义。阴性、阳性精神分裂症组两组比较，GABA和Glu、AchR、DA活动明显异常，差异具有统计学意义。PANSS总分与Ach、DA有相关性，阳性量表分与GABA、Ach、AchR、DA有相关性，阴性量表分与Glu、5-HT、DA有相关性，精神病理分与AchR、DA有相关性。结论阳性症状可能与GABA、Ach、AchR、DA具有相关性，阴性症状可能与Glu、5-HT、DA具有相关性。ET检测可作为诊断精神分裂症的依据之一。     

非痴呆性血管性认知功能障碍患者的脑电超慢涨落图表现

目的探讨主诉记忆力减退的非痴呆性血管性认知功能障碍(VCIND)患者脑内神经递质活动的变化及意义。方法选择2008—2012年第二炮兵总医院神经内科门诊患者716例,其中主诉记忆力减退的VCIND组370例,正常对照组346例。采用简易精神状态量表(MMSE)、蒙特利尔认知测评量表(MoCA)进行认知评估。应用脑电超慢涨落(EFG)分析仪测定S1γ-氨基丁酸(GABA)、S2谷氨酸(Glu)、S4 5-羟色胺(5-HT)、S5乙酰胆碱(Ach)、S7去甲肾上腺素(NE)、S11多巴胺(DA)等脑神经递质的活动。结果观察组GLU、5-HT的活动存在异常,GLU显著高于对照组(P<0.05),5-HT显著低于对照组(P<0.05);GABA、Ach、NE、DA的活动与对照组比较,差异无统计学意义(P>0.05)。结论主诉记忆力减退的VCIND人群脑内神经递质谷氨酸、5-羟色胺活动异常。EFG分析可作为一种有效的VCIND辅助诊断方法。     

右美托咪定对顽固性原发性失眠患者的脑电超慢涨落图的影响

目的 观察右美托咪定睡眠诱导平衡治疗后顽固性原发性失眠患者脑内神经递质活动的变化.方法 对23例顽固性原发性失眠且内科治疗效果不佳的患者实施右美托咪定睡眠诱导平衡治疗,每日1h,持续3d,对照组23例患者采用常规方案治疗.采用阿森斯失眠量表及过度觉醒量袁评估患者治疗前后的主观症状变化,并采用脑电超慢涨落技术对治疗前后的脑内神经递质分别进行检测.结果 治疗后治疗组阿森斯失眠量表及过度觉醒量表指标分值明显改善,治疗前患者脑内5-羟色胺活动水平偏低,去甲肾上腺素活动水平偏高,经睡眠诱导平衡治疗后5-羟色胺活动水平升高,去甲肾上腺素活动水平降低,差异具有统计学意义（P＜0.05）,余神经递质活动水平无明显变化,差异无统计学意义（P＞0.05）,且无严重治疗不良反应.结论 顽固性原发性失眠患者脑内神经递质存在5-羟色胺活动水平偏低,去甲肾上腺素活动水平偏高,右美托咪定睡眠诱导平衡术治疗可以调节它们的活动水平,同时患者的失眠症状及过度觉醒表现也有所改善.     

失眠患者血清钙调蛋白及GABA/Glu水平检测及其意义

目的检测血清钙调蛋白(Ca M)及γ-氨基丁酸(GABA)、谷氨酸(Glu)、GABA/Glu在失眠患者血清中的水平,探讨其与失眠的相关性。方法采用病例对照研究,收集符合入选标准的119例失眠患者作为研究组,收集122例健康体检者作为健康对照组。运用酶联免疫吸附法(ELISA法)检测所有入组者血清Ca M、GABA、Glu、GABA/Glu水平,并分析Ca M水平与GABA/Glu的相关性。结果 (1)失眠组患者与对健康照组相比,血清Ca M、GABA、GABA/Glu水平降低,Glu水平升高,有统计学意义(P 0.05)。(2)失眠患者血清Ca M水平与GABA/Glu水平呈正相关(r=0.475,P 0.01)。结论 Ca M下调增加失眠的风险,其机制可能与下调GABA/Glu水平有关。     

贝美格致痫大鼠皮层、海马γ—氨基丁酸和谷氨酸免疫反应细胞的改变

目的 γ－氨基丁酸（GABA）和谷氨酸（Glu）是脑内重要的抑制性和兴奋性神经递质，二者与癫痫发作密切相关，为了阐明癫痫发病的病理生理机制。方法 我们采用免疫细胞化学及PAP法，观察了贝美格（Bemegride,Be)腹腔致痫大鼠顶叶大脑皮层、海马CA1、CA3、齿状回Glu和GABA免疫反应细胞的改变。结果 图像分析结果显示：Be致痫组大脑皮层、海马Glu免疫反应平均阳性细胞数及光密度较正常对照组明显增加（P＜0．01）；GABA细胞数及光密度减少（P＜0．01）。结论 提示贝美格致痫作用与调节脑内GABA和Glu系统的兴奋性有关。     

脑涨落图检测脑梗死患者神经递质功率变化的特点

背景：脑涨落图分析技术是近几年来中国首创的一种无创伤性的脑功能检测方法,可通过测定脑电波中优势超慢波的功率,反映脑内神经递质含量。 目的：利用脑涨落图机观察脑梗死患者发病早期神经递质功率变化的特点。 设计、时间及地点：病例-对照分析,于2005-08/2006-03在中山大学孙逸仙纪念医院神经科完成。 对象：纳入脑梗死患者30例,病程3 h~2 d;以30例健康体检者为对照组。受试者均知情同意,并签署同意书。 方法：应用脑涨落图机收集30例脑梗死患者发病第1,3天、第六七天的神经递质功率信息,与健康体检者的脑电功率进行比较,分析脑梗死患者神经递质功率的变化特点。 主要观察指标：对照组和脑梗死组发病后不同时间脑涨落图中各神经递质功率、运动指数、兴奋抑制指数、血管舒缩指数及熵值。 结果：与对照组比较,脑梗死患者脑内神经递质γ-氨基丁酸、谷氨酸、兴奋递质3、5-羟色胺、乙酰胆碱、兴奋递质6、去甲肾上腺素、多巴胺、抑制递质13的功率在发病第1天均显著降低（P < 0.05）。发病第3天,脑梗死患者脑内神经递质γ-氨基丁酸与谷氨酸功率显著高于对照组（P < 0.05）,其他递质功率与总功率与对照组差异无显著性意义（P > 0.05）。发病第六七天,脑梗死患者脑内所有神经递质功率与对照组差异无显著性意义（P > 0.05）。 结论：γ-氨基丁酸及谷氨酸功率在脑梗死早期有一急剧升高再降至正常的过程。     

不同类型精神分裂症患者脑内神经递质活动的超慢涨落图分析

目的探讨脑电超慢涨落图（ET）与阴性、阳性精神分裂症异质性的关系。方法对首次发病未用药精神分裂症患者50例按PANSS量表复合分〉0分或〈0分为精神分裂症阳性组（23例）和精神分裂症阴性组（27例）,进行脑电超慢涨落图检测。结果阴性、阳性精神分裂症组与正常对照组相比,NE、5-HT活动显著降低,而DA活动则显著升高,差异具显著意义;阴性、阳性精神分裂症组比较,DA活动明显异常,差异具显著意义。结论ET检测可作为诊断精神分裂症的参考。     

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.