脑梗死患者血清细胞因子和C-反应蛋白水平的变化及其意义

目的观察脑梗死(CI)患者血清细胞因子——白介素-1β(IL-1β)、IL-6、肿瘤坏死因子-α(TNF-α)及C-反应蛋白(CRP)水平的变化及其意义。方法应用放射免疫法测定合并糖尿病(DM)CI患者(DMCI组,30例)、非DM的CI患者(NDMCI组,30例)、DM患者(DM组,20例)和正常对照组(20人)血清IL-1β、IL-6、TNF-α水平;应用免疫比浊法测定血清CRP水平,根据改良爱丁堡+斯堪的那维亚卒中量表神经功能缺损程度评分对CI患者按病情进行分组。结果DMCI组、NDMCI组及DM组血清IL-1β[(0.60±0.04)ng/ml、(0.33±0.03)ng/ml、(0.30±0.02)ng/ml]、IL-6[(231.07±7.68)pg/ml、(141.34±6.50)pg/ml、(118.92±5.82)pg/ml]、TNF-α[(2.70±0.11)ng/ml、(1.85±0.11)ng/ml、(1.21±0.13)ng/ml]及CRP[(7.44±0.26)ml/L、(4.67±0.21)mg/L、(4.54±0.24)mg/L]水平显著高于正常对照组[(0.20±0.03)n...     

脑梗死后癫(癎)患者血清细胞因子水平的改变

目的 研究脑梗死后癫(癎)患者血清细胞因子水平的改变.方法 应用放射免疫法检测87例脑梗死后癫癎患者(脑梗死癫(癎)组)和75名健康体检者(正常对照组)的血清肿瘤坏死因子α(TNF-α),白细胞介素(IL)-2和IL-6水平.结果 脑梗死癫(癎)组血清TNF-α[(2.5±0.57)ng/L]、IL-2[(9.0 4-0.83)ns/L]及IL-6[(97.5±3.1)ng/L]水平明显高于正常对照组[TNF-α(0.89 4-0.36)ng/L,IL-2(4.3±1.5)ng/L,IL-6(13.3 4-11.1)ng/L](均P＜0.01).结论 脑梗死后癫(癎)患者的血清细胞因子TNF-α、IL-2及IL-6水平显著升高,提示细胞因子可能在脑梗死后癫(癎)的发病中起重要作用.     

急性腔隙性脑梗死患者血清C反应蛋白和白介素-8水平的变化及临床意义

目的 探讨急性腔隙性脑梗死患者血清高敏C反应蛋白(hs-CRP)、白介素-8水平(IL-8) 的变化及其在发病机制中的作用.方法 分别检测36例腔隙性脑梗死和36例脑梗死患者及36例健康对照者血清hs-CRP和IL-8含量.结果 腔梗组和脑梗组hs-CRP含量分别为(10.42±0.68)mg/L和(18.45±1.28)mg/L,均显著高于对照组的(1.28±0.47)mg/L(P<0.01),CI组hs-CRP含量亦显著高于健康对照组(P<0.01);腔梗组和脑梗组IL-8含量分别为(29.65±18.24)ng/ml和(36.57±19.01)ng/ml,显著高于对照组的(25.98±16.87)ng/ml(P<0.01).在脑梗患死者中,大面积脑梗死组(≥9ml,n=16)hs-CRP为(21.36±1.48)mg/L,显著高于小面积脑梗死组(<9ml,n=20)的(15.30±0.97)mg/l(P<0.01),2组IL-8含量分别为(38.1±19.87)ng/ml和(33.45±18.67)ng/mL,差异亦有统计学意义(P<0.01).结论 炎症过程参与了脑小血管病变;hs-CRP和IL-8水平与脑缺血程度以及脑的小血管病变范围密切相关.hs-CRP 及IL-8是预测脑梗死患者病情严重程度的重要生化指标.     

慢性鼻-鼻窦炎与动脉粥样硬化性脑梗死相关性研究

目的探讨慢性鼻-鼻窦炎与血浆炎症指标和脑梗死发生的相关性。方法将入选的95例患者分为单纯脑梗死组(A组)、慢性鼻-鼻窦炎合并脑梗死组(B组)及正常对照组(C组),分别检测各组中CRP、TNF-α和IL-6的血浆含量。结果 A组的CRP、TNF-α和IL-6分别为(18.72±0.13)mg/L、(93.23±40.89)ng/IL和(18.23±3.42)ng/IL;B组分别为(28.76±0.89)mg/L、(126.32±34.64)ng/IL和(31.52±5.42)ng/IL;A组和B组的CRP、TNF-α和IL-6的表达水平均明显高于C组(P0.05),其中B组上述各炎症因子表达水平最高(P0.05)。结论慢性鼻-鼻窦炎与血浆中炎症指标的表达水平增高均与脑梗死的发生存在相关性。     

进展性脑梗死患者血清超敏C反应蛋白水平的变化及其临床意义

目的探讨进展性脑梗死患者血清超敏C反应蛋白(hs-CRP)水平的变化及其临床意义。方法检测63例脑梗死患者(25例进展性脑梗死、38例完全性脑梗死)和73名健康对照者(正常对照组)的血清hs-CRP含量。结果脑梗死患者的血清hs-CRP水平[(5.69±3.78)mg/L]明显高于正常对照组[(0.85±0.47)mg/L](P<0.01);进展性脑梗死组血清hs-CRP水平[(7.55±4.25)mg/L]明显高于完全性脑梗死组[(4.52±2.96)mg/L](P<0.01)。结论脑梗死患者血清hs-CRP水平明显升高,进展性脑梗死患者较完全性脑梗死患者血清hs-CRP水平升高更明显;提示hs-CRP参与了脑梗死的发生与发展过程。     

洛伐他汀对颈动脉粥样硬化斑块、血脂及血清C-反应蛋白水平的影响

目的 观察洛伐他汀对脑梗死患者颈动脉粥样硬化斑块、血脂及血清C-反应蛋白(CRP)水平的影响.方法 120例脑梗死合并颈动脉粥样硬化斑块患者随机分为洛伐他汀组和对照组.两组在低脂饮食的基础上,洛伐他汀组口服洛伐他汀20 mg每日1次,共6个月;观察两组治疗8周及 6个月时颈动脉粥样硬化斑块积分、血清CRP及血脂水平的变化.结果 (1)治疗6个月时,洛伐他汀组颈动脉粥样硬化斑块积分(4.20±3.77) 明显低于治疗前(4.77±2.31)及对照组(6.86±1.89)(均P<0.05);(2)治疗8周时,洛伐他汀组血清CRP水平[(6.37±2.16)mg/L]明显低于治疗前 [(16.35±5.18)mg/L] 及对照组[(16.30±4.84)mg/L](均P<0.05);(3)与治疗前及对照组比较,治疗8周及6个月时,洛伐他汀组血总胆固醇、三酰甘油及低密度脂蛋白胆固醇水平明显降低,高密度脂蛋白胆固醇明显升高(均P<0.05).结论 长期服用洛伐他汀可稳定甚至缩小颈动脉粥样硬化斑块,降低CRP及血脂水平,有助于预防脑卒中复发.     

IL-6 TNF-α hsCRP联合检测在急性脑梗死临床诊断中的应用

目的探讨联合检测急性脑梗死患者血清白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、超敏C反应蛋白(hsCRP)水平在临床诊断中的价值。方法采用ELISA法检测78例急性脑梗死患者发病24h内和50例健康体检者的血清IL-6、TNF-α、hsCRP水平。结果急性脑梗死患者血清IL-6、TNF-α、hsCRP水平分别为(13.24±2.30)ng/L、(78.45±12.09)ng/L、(17.26±3.64)mg/L,均高于健康体检者的(2.09±0.51)ng/L、(12.34±2.12)ng/L、(1.09±0.34)mg/L,差异有统计学意义(P0.05)。血清IL-6、TNF-α、hsCRP水平与急性脑梗死的严重程度有关(P0.05)。结论血清IL-6、TNF-α、hsCRP水平在急性脑梗死发病后明显升高,且随病情的加重而升高,三者联合检测有助于急性脑梗死的早期确诊及病情评估。     

伴颈动脉粥样硬化的急性脑梗死患者胰岛素抵抗与TNF-α关系的临床研究

目的探讨肿瘤坏死因子α(TNF-α)与胰岛素抵抗(IR)在伴颈动脉粥样硬化(CAS)的急性脑梗死中的作用机制及二者之间的关系。方法比较44例伴CAS的急性脑梗死患者与80例健康对照组中空腹血糖(FPG)、空腹血清胰岛素(FINS)、胰岛素敏感指数(ISI)、胰岛素抵抗指数(HOMA-IR)、TNF-α、体重指数(BMI)等6个因素之间有无差异,并了解IR与TNF-α的相关性。结果伴CAS的急性脑梗死组与对照组相比,FPG、FINS、HOMA-IR、TNF-α明显高于对照组,ISI明显低于对照组(P<0.01或P<0.05);脑梗死组中,ISI与TNF-α呈显著负相关(r=-0.494,P<0.01)。结论在伴有CAS的急性脑梗死中同时存在IR及TNF-α升高,IR程度与TNF-α呈正相关。     

急性腔隙性脑梗死患者血清C-反应蛋白和白介素-8水平的变化及临床意义

目的 探讨急性腔隙性脑梗死患者血清高敏C-反应蛋白(hs-CRP)、白介素-8水平(IL-8) 的变化及在发病机制中的作用.方法 分别检测36例腔隙性脑梗死、36例脑梗死和36例健康对照者血清hs-CRP和IL-8含量.结果 腔梗组和脑梗组hs-CRP含量分别为(10.42±0.68)、(18.45±1.28)mg/L,均显著高于对照组的(1.28±0.47)mg/L(P＜0.01),CI组hs-CRP含量亦显著高于健康对照组(P＜0.01);腔梗组和脑梗组IL-8含量分别为(29.65±18.24)、(36.57±19.01)ng/ml,显著高于对照组的(25.98±16.87)ng/ml(P＜0.01),在脑梗患者中,大面积脑梗死(≥9ml)hs-CRP为(21.36±1.48)mg/L,显著高于小面积脑梗死组(<9ml)的(15.30±0.97)mg/L(P＜0.01),2组IL-8含量分别为(38.1±19.87)、(33.45±18.67)ng/ml,差异亦有统计学意义(P＜0.01).结论 炎症过程参与了脑小血管病变;hs-CRP和IL-8水平与脑缺血程度以及脑的小血管病变范围密切相关.hs-CRP 及IL-8是预测脑梗死患者病情严重程度的重要生化指标.     

急性脑卒中患者血清红细胞生成素水平改变及其意义

目的探讨急性脑卒中患者血清红细胞生成素(EPO)水平改变及其临床意义。方法应用放射免疫法检测60例脑梗死(脑梗死组)、45例脑出血(脑出血组)和40例其他神经系统疾病患者(对照组)的血清EPO水平。用美国国立卫生研究院卒中量表(NIHSS)对急性脑卒中患者进行评分。结果脑梗死组和脑出血组血清EPO水平[(1.64±0.41)ng/ml,(1.59±0.54)ng/ml]显著高于对照组[(1.17±0.86)ng/ml](均P<0.05),脑梗死组及脑出血组的NIHSS评分[(10.42±3.75)分,(11.58±4.16)分]与血清EPO水平呈负相关(r=-0.482,r=-0.537,均P<0.05)。结论急性脑卒中患者的血清EPO水平明显升高,并且病情越重的患者血清EPO水平越低。     

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.     

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.     

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.     

Neonatal Seizures: Problems in Diagnosis and Classification

Summary: The clinical identification of neonatal seizures is critical for the recognition of brain dysfunction; however, diagnosis is often difficult because of the poorly organized and varied nature of these behaviors. Current classification systems are limited in their ability to communicate motor, autonomic, and electroencephalo-graphic features of seizures precisely and to provide a basis for uniform effective diagnosis, therapy, and determination of prognosis. Recent investigations of neonates, utilizing bedside electroencephalographic/polygraphic/ video monitoring techniques, have provided the basis for improved diagnosis and classification of seizures in the newborn. These studies have demonstrated that not all clinical phenomena currently considered to be seizures require electrocortical epileptiform activity for their initiation or elaboration. In addition, the specific clinical character of the phenomena considered to be seizures, the clinical state of the infant, and the character of the EEG indicate the probable pathophysiological mechanisms involved and suggest probable etiologies, prognosis, and therapy. Similarities between animal models that demonstrate reflex physiology and neonates with motor automatisms and tonic posturing suggest that these clinical behaviors may not be epileptic in origin but, rather, primitive movements of progression and posture mediated by brainstem mechanisms. Although not all clinical behaviors currently considered to be neonatal seizures may have similar pathophysiological mechanisms, they are clinically significant because they all indicate brain dysfunction.     

Valproate Monotherapy in the Management of Generalized and Partial Seizures

Summary: For decades, therapeutic tradition has promoted the concept of polypharmacy in the management of epilepsy. In recent years, however, studies have shown that, for most patients, monotherapy can provide comparable or better seizure control than administration of multiple anticonvulsants, while diminishing the potential for adverse reactions, drug interactions, and poor compliance. Valproate is an important monotherapeutic agent that is highly effective in the control of idiopathic primary and secondarily generalized epilepsies, and partial seizures that do not generalize. Comparative studies have found that valproate is at least as effective as phenytoin and carbamazepine in the treatment of generalized and partial seizures. Given the similar efficacy, other factors such as pharmacokinetics and side effects may therefore determine anticonvulsant selection for monotherapy.     

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.     

Un nouveau cadre conceptuel de travail pour la psychiatrie

In an attempt to place psychiatric thinking and the training of future psychiatrists more centrally into the context of modern biology, the author outlines the beginnings of a new intellectual framework for psychiatry that derives from current biological thinking about the relationship of mind to brain. The purpose of this framework is twofold. First, it is designed to emphasize that the professional requirements for future psychiatrists will demand a greater knowledge of the structure and functioning of the brain than is currently available in most training programs. Second, it is designed to illustrate that the unique domain which psychiatry occupies within academic medicine, the analysis of the interaction between social and biological determinants of behavior, can best be studied by also having a full understanding of the biological components of behavior.