缺血性脑卒中患者P选择素、溶酶体蛋白表达的变化及其临床意义

目的　探讨缺血性脑卒中患者P选择素(CD62P)、溶酶体蛋白(CD63)表达的规律及其临床意 义。方法　运用流式细胞术检测168例缺血性脑卒中患者(急性期及恢复期)及40名健康对照者CD62P、CD63 的表达,并与神经功能缺损程度评分(NDS)进行相关分析。结果　(1)缺血性脑卒中患者急性期CD62P、CD63 表达[(9.48±1.24)%、(8.36±1.18)%]显著高于其恢复期[(5.73±1.27)%、(4.21±1.20)%]及健康对 照组[(1.59±0.56)%、(0.92±0.38)%](均P<0.01),恢复期CD62P、CD63表达仍高于对照组(P<0.01); (2)缺血性脑卒中组急性期患者按牛津郡社区卒中计划分为4个亚型,CD62P、CD63表达在完全前循环梗死 (TACI)组[(16.45±1.13)%、(15.59±1.28)%]明显高于部分前循环梗死(PACI)组[(10.63±1.18)%、 (9.38±1.14)%]、后循环梗死(POCI)组[(10.54±1.14)%、(9.33±1.13)%]及腔隙性梗死(LACI)组 [(6.59±1.35)%、(5.53±1.20)%](均P<0.01),PACI组及POCI组明显高于LACI组(均P<0.01),而 PACI组及POCI组之间差异无显著性(P>0.05);(3)CD62P、CD63表达与NDS呈显著直线正相关(r=0.84、 r=0.817,均P<0.01)。结论　缺血性脑卒中患者急性期CD62P、CD63表达显著升高,可能参与了缺血性脑损 伤形成的病理过程,并间接反映其病情程度;恢复期CD62P、CD     

血小板激活及血小板参数变化在脑梗死发病机制中的作用

目的研究血小板激活以及血小板参数变化在脑梗死发病机制中的作用。方法采用流式细胞术测定急性脑梗死患者168例和健康对照者40名外周血P选择素(CD62p)、溶酶体蛋白(CD63)的阳性表达率,同时测定血小板计数(PLT)、血小板平均体积(MPV)和血小板最大聚集率(MAR)。并进行比较及相关因素分析。结果(1)脑梗死患者CD62p、CD63及MPV、MAR明显高于健康对照组,并且上述指标急性期均高于恢复期(均P<0·01);(2)全前循环梗死(TACI)亚型的脑梗死患者CD62p、CD63及MPV、MAR显著高于部分前循环梗死(PACI)、后循环梗死(POCI)及腔隙性梗死(LACI)亚型,在PACI及POCI亚型中上述各测定值较LACI亚型显著增高,差异均具有显著性(均P<0·01);而在PACI及POCI亚型之间差异并无显著性(P>0·05);(3)PLT在脑梗死患者急性期、恢复期与健康对照组之间以及牛津郡社区卒中项目(OCSP)各亚型之间差异无显著性(均P>0·05)。(4)CD62p、CD63呈显著正相关(r=0·826,P<0·01),且与MPV及MAR亦呈明显正相关(r=0·703、0·698,均P<0·01);但与PLT之间无相关性(均P>0·05)。结论脑梗死患者血小板的大量激活及其体积和最大聚集率的升高参与了脑梗死的病理过程,监测MPV和MAR较PLT更能反映脑梗死的病情程度,为应用抗血小板聚集药物提供依据。     

OCSP分型与脑梗死急性期神经功能缺损和预后的相关性研究

目的研究脑梗死急性期OCSP分型与神经功能缺损和预后的关系.方法连续收集首次发病的急性脑梗死(发病时间在10 d以内)患者160例,按OCSP分型分为完全前循环梗死(TACI)、部分前循环梗死(PACI)、腔隙性脑梗死(LACI)、后循环梗死(POCI),比较斯堪的纳维亚神经功能缺损评分,入组后30 d、6个月的患者病死率、脑卒中复发率(包括缺血性和出血性)和日常生活能力.结果急性期神经功能缺损以TACI最重,POCI、PACI次之,LACI最轻,入组后30 d的患者病死率为TACI＞POCI＞PACI＞LACI,6个月时病死率仍然是TACI＞POCI＞PACI＞LACI,而6个月内脑卒中复发率是PACI＞POCI＞LACI＞TACI,存活6个月者残疾程度TACI最重(重度依赖),其余3个亚型均为轻度依赖.结论脑梗死急性期不同OCSP分型之间的脑梗死患者急性期神经功能缺损、30 d及6月时预后存在差异,不同的OCSP分型可以反映脑梗死急性期神经功能缺损的严重程度和预后,OCSP分型有利于脑梗死急性期治疗和康复方法的选择.     

血清缺血修饰清蛋白与急性脑梗死的相关性研究

目的探讨血清缺血修饰清蛋白与急性缺血性脑卒中各亚型及患者早期预后的相关性。方法选取我院2013-04-2016-03收治的符合研究标准的104例急性缺血性脑卒中患者为研究组,另选取同期门诊体检健康者54例为对照组。根据英国牛津郡社区脑卒中分型(OCSP)标准将104例急性缺血性脑卒中患者分为腔隙性梗死(LACI)组(n=25)、后循环梗死(POCI)组(n=25)、部分前循环梗死(PACI)组(n=28)、完全前循环梗死(TACI)组(n=26)。抽取各组血清进行检测,对比不同亚型急性缺血性脑卒中患者血清缺血修饰清蛋白水平,并与对照组比较,统计不同亚型急性缺血性脑卒中患者治疗前后神经功能缺损评分(NIHSS)及日常生活活动能力评分(Barthel指数)变化情况。结果 LACI组、POCI组、PACI组、TACI组血清缺血修饰清蛋白水平均明显高于对照组,差异有统计学意义(P0.05);TACI组血清缺血修饰清蛋白水平明显高于LACI组、POCI组、PACI组,差异有统计学意义(P0.05);治疗前各组NIHSS评分及Barthel指数对比差异无统计学意义(P0.05),治疗后各组均较治疗前改善,且TACI组与其余3组对比差异有统计学意义(P0.05)。结论血清缺血修饰清蛋白作为急性缺血性脑卒中分型参考指标,其表达水平与患者预后具有密切相关性,血清缺血修饰清蛋白水平越高,预后效果越差。     

急性脑梗死不同临床亚型患者血清髓鞘碱性蛋白的变化

目的 观察不同临床类型急性脑梗死(ACI)患者血清髓鞘碱性蛋白(MBP)水平变化,探讨MBP与美国国立卫生研究所卒中量表(NIHSS)评分之间的关系.方法 208例ACI患者按照牛津郡社区卒中计划(OCSP)分型标准分为4组并行NIHSS评分,采用ELISA法检测血清MBP的含量;观察不同亚型ACI患者MBP含量的变化,分析MBP与NIHSS评分的相关性.结果 (1)本组OCSP各亚型构成比:完全前循环型(TACI) 13.46％、部分前循环型(PACI)30.29％、后循环型(POCI) 19.71％、腔隙性梗死型(LACI)36.54％;(2)OCSP分型中TACI、PACI及POCI亚型MBP含量升高,LACI变化不明显.与LACI比较,TACI、PACI及POCI有显著性差异(P＜0.05);(3)TACI、PACI中血清MBP含量与相应时间段NIHSS评分具有有相关性,相关系数为0.62、0.60 (P＜0.05);POCI和LACI中MBP与NIHSS之间相关性较差.结论 MBP随OCSP亚型的不同而变化.TACI、PACI、POCI亚型的缺血性卒中患者血清MBP可以作为病情、预后判断的一个参考依据.     

急性脑梗死患者临床分型及梗死面积与心电图改变的关系

目的 探讨急性脑梗死患者临床分型和梗死面积与心电图(ECG)改变的关系.方法 给216例急性脑梗死患者进行ECG检查,按牛津郡社区卒中项目(OCSP)分型和梗死面积分型,对各组患者的ECG检查结果进行分析比较.结果 OCSP分型完全前循环梗死(TACI)组、部分前循环梗死(PACI)组、后循环梗死(POCI)组和腔隙性梗死(LACI)组患者的ECG异常率分别是: 95. 5%、80.4%、62.5%和48.5%,TACI组和PACI组明显高于LACI组(P＜0.05～0.01);大中面积梗死组(83.7%)的ECG异常率明显高于小面积梗死组(60.4%)和腔隙性梗死组(53.2%)(P＜0.05～0.01);小面积梗死组的ECG异常率高于腔隙性梗死组(P＜0.05).OCSP和梗死面积分型各亚型组出现ST-T改变和心律失常的比率差异有统计学意义(P＜0.05～0.01).结论 急性脑梗死临床分型病情重和梗死面积大的患者ECG异常率高.     

急性脑梗死患者血清P-选择素和CRP含量动态变化研究

目的 探讨缺血性脑卒中患者血清P-选择素和C反应蛋白（CRP）含量的动态变化和临床意义.方法 分别运用酶联免疫吸附测定（ELISA）的方法和免疫透射比浊法检测30例脑梗死患者和30名健康对照者例健康对照者P-选择素、CRP的血清水平.结果 缺血性脑卒中患者急性期血清P-选择素和CRP水平显著高于其恢复期及健康对照组（均P＜0.01）,恢复期P-选择素和CRP水平仍高于健康对照组（P＜0.05）.不同体积脑梗死患者的P-选择素和CRP水平不同,大梗死灶组和中梗死灶组比小梗死灶组P-选择素和CRP水平明显升高,差异具有统计学意义（P＜0.01）.结论 P-选择素和CRP参与了缺血性脑卒中炎症反应和血小板活化的病理过程,血清P-选择素和CRP水平可作为缺血性脑血管病发生发展及病情监测的参考指标.     

脑梗死患者脂蛋白（α）及纤维蛋白原的变化和临床意义

目的：探讨脑梗死患者血清脂蛋白（α）[Lp(α)]和纤维蛋白原（FIB）的水平变化及临床意义。方法：随机选择36例急性期脑梗死患者测定血清Lp(α)和FIB，30例健康人作为对照组。结果：脑梗死急性期血清Lp(α)和FIB水平显著高于健康对照组（P＜0．05）；大面积脑梗死患者血清Lp(α)和FIB水平显著高于小面积脑梗死（P＜0．05）；Lp(α)和FIB间呈正相关（P＜0．01）。结论：脑梗死急性期血清Lp(α)和FIB水平增高；Lp（α）和FIB水平与梗死面积有关。Lp(α)和FIB可作为预防和治疗脑梗死的良好观测指标。     

脑梗死患者血清纤维蛋白原和D-二聚体含量的变化及其意义

目的　探讨脑梗死患者急性期、亚急性期和恢复期血清纤维蛋白原、D-二聚体含量的变化及其意义。方法　对 6 0例脑梗死患者急性期、亚急性期和恢复期纤维蛋白原、D-二聚体的含量进行测定 ,并与 30名健康对照者进行比较。结果　纤维蛋白原和 D-二聚体的含量在 3个阶段均较对照组显著升高 (P<0 .0 1) ,升高的程度与梗死体积密切相关 ;纤维蛋白原的含量在 3个阶段之间比较无显著性差异 (P>0 .0 5 ) ,而 D-二聚体的含量在亚急性期显著升高 (P<0 .0 5 ) ,恢复期开始下降。结论　缺血性脑血管疾病的发生和发展与凝血 -纤溶系统的异常有密切关系     

吞咽功能训练联合低频电刺激术治疗缺血性卒中吞咽障碍的疗效观察

目的探讨吞咽功能训练联合低频电刺激术对缺血性卒中患者吞咽障碍的疗效。方法共68例缺血性卒中合并吞咽障碍患者,分别予常规吞咽功能训练(包括吞咽训练和进食策略训练,对照组)及常规吞咽功能训练联合低频电刺激术(联合治疗组),于治疗前和治疗后15 d,采用视频透视吞咽检查(VFSS)和标准吞咽功能评价量表(SSA)评价患者吞咽功能。结果 34例予以常规吞咽功能训练,英国牛津郡社区脑卒中项目(OCSP)分型完全前循环梗死型(TACI型)12例、部分前循环梗死型(PACI型)8例、后循环梗死型(POCI型)10例、腔隙性梗死型(LACI型)4例;34例予以常规吞咽功能训练联合低频电刺激术,OCSP分型TACI型10例、PACI型7例、POCI型11例、LACI型6例。与治疗前相比,两组患者治疗后VFSS评分增加(P=0.003,0.000)、SSA评分减少(P=0.003,0.000);与对照组相比,联合治疗组患者VFSS评分增加(P=0.004)、SSA评分减少(P=0.020)。结论吞咽功能训练联合低频电刺激术对急性缺血性卒中患者吞咽障碍具有较好疗效,优于单纯吞咽功能训练。     

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.