进展性缺血性脑卒中影响因素的前瞻性研究

目的 探讨进展性缺血性脑卒中的危险因素.方法 前瞻性登记急性缺血性脑卒中患者并收集其临床资料.依据欧洲进展性卒中诊断标准将患者分组,对可能影响卒中进展的因素进行比较及多因素Logistic逐步回归分析.结果 共有569例患者纳入研究,其中127例归入进展性卒中组,442例归入非进展性卒中组.进展性卒中组患者的病程、伴糖尿病、心房纤颤史及脑卒中史、入院时发热、高血糖、合并并发症、入院时美国国立卫生研究院卒中量表及格拉斯哥昏迷量表评分与非进展性卒中组比较差异有统计学意义(均P<0.1).多因素Logistic逐步回归分析显示,糖尿病(RR=2.625,95%CI:1.422～4.844)、发热(RR=0.192,95%CI:0.075～0.491)、合并并发症(RR=2.442,95%CI:1.394～4.279)、神经功能缺损中度(RR=5.602,95%(CI:2.789～11.251)及重度(RR=24.734,95%CI:4.218～145.052)是进展性卒中的独立危险因素.结论 糖尿病、发热、合并并发症、中及重度神经功能缺损是缺血性脑卒中进展的独立危险因素.     

出血性进展性卒中的发生及危险因素的前瞻性研究

目的 观察出血性脑卒中患者中进展性卒中的发生情况及可能的影响因素.方法 前瞻性连续登记急性脑出血患者,根据欧洲进展性卒中诊断标准判定是否进展,对可能导致卒中进展的危险因素进行单因素和多因素分析.结果 共登记脑出血患者259例,符合纳入标准的有237例,其中75例为进展性卒中,发生率31.6%.对可能影响卒中进展的危险因素进行单因素和多因素分析,结果显示血肿扩大(RR 9.98, 95%CI 3.43, 29.02)、相对于轻度神经功能缺损的中度 (RR 0.04, 95%CI 0.01, 0.17) 和重度神经功能缺损 (RR 0.03, 95%CI 0.01, 0.17) 是卒中进展的独立危险因素.结论 急性脑出血患者中近三分之一出现神经功能进展,血肿扩大、神经功能缺损程度重与卒中进展独立相关.     

卒中后睡眠障碍相关危险因素的Meta分析

【摘要】
目的 通过对卒中后睡眠障碍相关文献进行分析,分析卒中后睡眠障碍的常见危险因素。
方法 采用Meta分析方法,对符合条件的11篇有关卒中后睡眠障碍危险因素的文献进行定量分析,对每个危险因素进行异质性检验以及合并优势比（odds ratio,OR）和95％可信区间（confidence interval,CI）的计算。
结果 有5个因素与卒中后睡眠障碍有统计学意义,分别是：习惯性打鼾（OR 14.77,95％CI 5.52～39.53）、高血压（OR 1.3,95％CI 1.03～1.66）、糖尿病（OR 1.41,95％CI 1.08～1.84）、饮酒（OR 1.59,95％CI 1.19～2.12）、皮质型卒中（OR 1.31,95％CI 1.06～1.63）,合并结果稳定性较好。尚不能确定性别（OR 1.12,95％CI 0.96～1.31）、高血脂（OR 0.96,95％CI 0.7～1.33）、吸烟（OR 1.27,95％CI 0.73～2.20）、卒中史（OR 1.05,95％CI 0.74～1.49）与卒中后睡眠障碍有关。
结论 现有的证据表明高血压、糖尿病、饮酒、习惯性打鼾及皮质型卒中是卒中后睡眠障碍的危险因素。     

脑卒中患者吞咽障碍恢复不良影响因素的Meta分析

目的 系统分析脑卒中患者吞咽障碍恢复不良的影响因素。方法 系统检索中国知 网、万方数据库、维普网、中国生物医学文献数据库、PubMed、Cochrane Library、Embase 数据库,收集 建库至 2022 年 12 月发表的脑卒中患者吞咽障碍恢复不良影响因素相关研究,使用 RevMan 5.4.1 软件 对纳入文献进行Meta分析。结果 共纳入 22 篇文献,4 248 例患者。Meta分析结果显示,年龄≥ 70 岁 （OR=1.53,95%CI：1.29～1.80）、美国国立卫生研究院卒中量表（NIHSS）评分≥ 8 分（OR=2.36,95%CI： 1.53～3.63）、改 良 Rankin 量 表（mRS）评 分 ＞ 0 分（OR=1.71,95%CI：1.40～2.09）、双 侧 卒 中（OR=4.85, 95%CI：2.62～8.97）、低密度脂蛋白（LDL）水平≥3 mg/L（OR=3.70,95%CI：2.46～5.56）、认知障碍（OR=6.23, 95%CI：0.98～39.58）、误吸（OR=4.47,95%CI：3.28～6.11）、气管插管（OR=2.70,95%CI：1.58～4.63）是脑 卒中患者吞咽功能恢复不良的危险因素（P＜ 0.05）;体重指数＞ 18.5 kg/m2 （OR=0.76,95%CI：0.67～0.86）、 Barthel 指数（BI）＞ 60 分（OR=0.37,95%CI：0.22～0.62）、功能独立性测评（FIM）评分＞ 20 分（OR=0.96, 95%CI：0.94～0.99）是脑卒中患者吞咽功能恢复不良的保护因素（P＜0.05）。结论 高龄、高NIHSS评分、 双侧卒中、低体重指数、高 mRS 评分、低 BI、低 FIM 评分、高 LDL 水平、合并认知障碍、误吸、气管插管是 脑卒中患者吞咽障碍恢复不良的危险因素,临床可结合影响因素完善吞咽障碍患者的管理措施。     

缺血性卒中患者吞咽障碍危险因素的meta分析

目的 系统分析缺血性卒中患者发生吞咽障碍的危险因素。 方法 计算机检索Cochrane Library、PubMed、Embase、Web of Science、中国知网、万方、维普等数据库, 检索建库至2020年2月关于缺血性卒中患者发生吞咽障碍危险因素的文献。采用纽卡斯尔-渥太华量 表对文献质量进行评价,纳入该量表≥7分的文献。采用RevMan 5.3软件进行meta分析,先对各影响 因素进行异质性评估,如无异质性,采用固定效应模型分析;如存在异质性,则采用随机效应模型分 析,计算各影响因素的合并MD 值或OR 值及95%CI。 结果 共纳入9篇文献,合计样本量为4095例,其中发生吞咽障碍患者981例（23.96%）。经 m eta分析结果显示,年龄（MD 4.98,95%CI 3.84～6.11,P ＜0.001）、高血压（OR 2.21,95%CI 1.44～3.38,P ＜0.001）、糖尿病（OR 1.79,95%CI 1.36～2.36,P＜0.001）、脑干卒中（OR 2.07, 95%CI 1.31～3.26,P =0.002）是缺血性卒中患者发生吞咽障碍的独立危险因素。 结论 对于缺血性卒中患者,年龄增长、高血压、糖尿病及脑干卒中是发生吞咽障碍的独立危险 因素,临床中应注意评估和早期干预吞咽障碍的危险因素。     

中国人群脂联素＋45位点基因单核苷酸多态性与缺血性脑卒中易感性的Meta分析

目的 通过Meta分析评估中国人脂联素基因＋45T＞G单核苷酸多态性（SNP）与缺血性脑卒中易感性的关系.方法 计算机检索Pubmed、Cochrane、中国期刊全文数据库（CNKI）及万方数据库中关于中国人群脂联素基因＋ 45T＞G SNP与缺血性脑卒中的相关性研究,对符合纳入标准的文献采用Rev Man5.2软件进行分析.结果 共纳入6篇文献,1604例患者.分析显示如下遗传模型中的差异明显,即等位基因模型（G VS.T）：OR=1.34,95％CI（1.04,2.72）;共显性模型（GG VS.TT）：OR=1.71,95％CI （1.27,2.30）;隐性模型（GG VS.F＋ TT）：OR=1.82,95％ CI（1.18,2.82）;显性模型（TG＋ GGVS.TT）：OR=1.22,95％CI （1.05,1.42）.结论 中国人群脂联素基因＋45T＞G SNP与缺血性脑卒中易感性相关,G等位基因可能为缺血性脑卒中的危险因素.     

卒中后抑郁相关影响因素的Meta分析

目的 探索脑卒中相关危险因素，为卒中后抑郁的早期诊断及预防决策提供依据。方法 标 准化检索万方、知网、维普、Medline、Cochrane 和Embase 有关卒中后抑郁相关性研究的文献，进一步提 取文献中相关因素的比值比（OR）及95%CI, 合并各个相关因素的OR值及95%CI以评估各因素在卒中后 抑郁中的作用。通过Egger''s检验和敏感性分析评估各相关因素的偏倚风险和结果稳定性。结果 Meta 分析结果显示基底节区梗死（OR=2.83）、多病灶（OR=2.76）、额叶梗死（OR=2.47）、高改良Rankin 量表（mRS） 评分（OR=2.17）、缺乏家庭支持（OR=1.48）、高水平超敏C 反应蛋白（OR=1.35）、女性（OR=1.66）、高水平同型 半胱氨酸（OR=1.17）、高水平瘦素（OR=1.16）、高体质指数（BMI）（OR=1.16）、年龄（OR=1.07）为卒中后抑郁 的危险因素，而高受教育水平（OR=0.91）可能对卒中后抑郁具有保护作用。结论 高水平瘦素、高水平 BMI、高mRS 评分、多病灶、基底节区梗死、额叶梗死、缺乏家庭支持、女性、高水平超敏C 反应蛋白、高 水平同型半胱氨酸、年龄是卒中后抑郁的危险因素，高受教育水平可能对卒中后抑郁具有保护作用。     

卒中后疲劳危险因素的系统评价

目的 系统评价卒中后疲劳危险因素，为卒中后疲劳的防治及健康教育提供参考依据。 方法 计算机检索The Cochrane Library、PubMed、Web of SCIence、EMbase、CNKI、WanFang Data和VIP 数据库，搜集有关卒中后疲劳相关危险因素的病例-对照研究、队列研究、横断面研究，检索时限均 为建库至2019年10月30日。由2名研究者独立筛选文献、提取资料并评价纳入研究的偏倚风险后，采 用RevMan5.3进行Meta分析。 结果 共纳入14 项研究，包括3 2 01例患者。M e t a分析结果显示：卒中前疲劳（O R 5.9 3， 95%CI 3.41～10.32，P＜0.001）、抑郁症（OR 2.48，95%CI 1.83～3.36，P＜0.001）、女性（OR 1.67， 95%CI 1.24～2.26，P＜0.001）、家庭功能障碍（OR 2.57，95%CI 1.86～3.57，P＜0.001）、mRS评分 （OR 2.65，95%CI 2.04～3.45，P＜0.001）、冠心病（OR 3.41，95%CI 1.97～5.90，P＜0.001）、不能自 理（OR 4.32，95%CI 2.47～7.54，P＜0.001）、高脂血症（OR 2.27，95%CI 1.20，4.27，P =0.01）、镇静药 物使用（OR 4.10，95%CI 2.14～7.87，P＜0.001）是卒中后疲劳的危险因素；卒中前规律运动（OR 0.50， 95%CI 0.36～0.70，P＜0.001）是卒中后疲劳的保护因素。 结论 本研究结果显示，性别（女性）、卒中前疲劳、抑郁、家庭功能障碍、mRS评分、冠心病、自理 能力差、高脂血症、镇静药物使用可能是卒中后疲劳的危险因素，其余风险因素相关性有待进一步研 究。受纳入研究数量和质量的限制，上述结论尚待更多高质量研究予以验证。     

大脑中动脉分布区缺血性卒中患者的临床和影像学特征及复发危险因素

目的 分析大脑中动脉（middle cerebral artery，MCA）分布区非心源性缺血性卒中患者的临床和影像 学特征及复发的危险因素。 方法 连续入选发病7 d以内的MCA分布区非心源性缺血性卒中患者。收集患者的人口学信息、血管 病的危险因素和发病时的主要症状及体征，评价患者的头颅磁共振影像包括急性梗死灶的部位、 数量、分布特征、责任动脉有无狭窄、缺血性卒中的病因分型。随访患者1年内有无缺血性卒中或短暂 性脑缺血发作（transient ischemic attack，TIA）复发，通过多元Logistic回归分析患者复发的危险因素。 结果 研究共入组926例患者，责任MCA狭窄≥70%的患者（447例）常见多发梗死灶（338例，75.6%） 和分水岭梗死（317例，70.9%），而责任MCA无狭窄或狭窄程度<70%患者（479例）常见MCA穿支分 布区单发梗死灶（247例，55.3%）。冠状动脉粥样硬化性心脏病[比值比（odds ratio，OR）7.55，95%可 信区间（confidence interval，CI）2.85～20.0，P <0.001]、缺血性卒中病史（OR 3.49，95%CI 1.52～8.01， P =0.003）、缺血性卒中发病前3个月内反复TI A史（OR 22.7，95%CI 8.35～61.6，P <0.001）、新发梗死 灶为多发（OR 5.26，95%CI 1.33～20.8，P =0.018）是患者1年内缺血性卒中或TIA复发的危险因素。 结论 对于非心源性缺血性卒中患者，MCA分布区梗死灶的分布特征与MCA狭窄程度有关。新发梗 死灶为多发、既往有缺血性心脑血管病病史的患者1年缺血性卒中或TIA复发风险高。     

进展性缺血性脑卒中相关危险因素分析

目的探讨进展性缺血性脑卒中发病的相关危险因素,为其预防和治疗提供依据。方法选取2011-06—2013-05我院收治的进展性缺血性脑卒中85例,非进展性缺血性脑卒中98例;通过查阅患者病历、进行问卷调查和血清学检测,分析进展性缺血性脑卒中发病的危险因素。结果 2组患者的糖尿病史、高血压史、高血脂史、伴颈动脉粥样硬化比例有显著差异(P0.05),2组患者的空腹血糖、白细胞、血清胆固醇、高密度脂蛋白、低密度脂蛋白、甘油三脂、纤维蛋白原也具有显著性差异(P0.05)。结论糖尿病史、高血压史、高血脂史伴颈动脉粥样硬化的患者是进展性缺血性脑卒中发病的高危人群,高血糖、高白细胞、高胆固醇、低高密度脂蛋白、高低密度脂蛋白、高甘油三酯、高纤维蛋白原是进展性缺血性脑卒中的危险因素。     

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.     

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.     

Une phénoménologie de la dépendance à l'alcool. Une expérience primordiale de la « nostrité »

The phenomenological approach to alcoholism interestingly focuses on specific dynamics of interpersonal relationships displaying the founding of the Self from a primary “us” and its original basis in the human feast. Priorities for treatment intervention recommend to involve social setting and relationships of the patients, reaching their active participation to a motivational and long term group treatment, underlying the specific therapeutic effect of world exchanges. Biopsychosocial determination of alcoholism could be primarily based on components of interpersonal relationships. Regarding social background, drinking is one of the most famous supports for the achievement of the feast, a founding marker of present time. Taking an existential point of view, the feast appears as the heart of mankind because it presents a primary “us”, a plural state which indicates the beginning and founding of the Self from the others. During the feast, we regularly have to reach our Self from the “us” while avoiding two main dangers, drunkenness, an increase in the dizziness of upright verticality, and addiction, an opposite vertical surrender to alcohol and falling into in the alcoholic relapse, both situations imply a spatial domination and the disappearance of others. Treatment programs of alcohol addicts need to integrate the necessity of reaching the existential basic trust from the support of a group to the appropriation of the community which can be defined as an original “usness”.