高血压患者平均动脉压与脑卒中的相关危险因素分析

目的探讨脑卒中发病的危险因素,分析高血压史和平均动脉压水平与脑卒中发病的相关性。方法对5 434例中老年人群进行基线调查,根据有无脑卒中分为脑卒中组和非脑卒中组,记录其高血压史、年龄、平均动脉压、性别、体重指数等一般资料,采用单因素分析探讨脑卒中的危险因素。高血压史和平均动脉压与脑卒中的相关性采用分层单因素分析,高血压史分为无高血压组、20a以下组和20a以上组3个亚组;平均动脉压分成75mmHg组、正常组和165mmHg组3个亚组。结果高血压病程、平均动脉压异常、年龄、性别等为脑卒中的危险因素;高血压史亚组组间比较,P0.01;平均动脉压75mmHg组与平均动脉压正常组比较,P0.01;平均动脉压正常组与平均动脉压165mmHg组比较,P0.01;平均动脉压75mmHg组与平均动脉压165mmHg组比较,P0.05。结论高血压史与脑卒中的发生率密切相关,病史越长,脑卒中发生几率越高;平均动脉压异常是脑卒中的危险因素,过高或过低对脑卒中发病率的影响不明显。     

脑卒中患者相关危险因素分析

目的探讨脑卒中发病的危险因素。方法对2 715例中老年人群进行调查,根据受试者有无脑卒中病史分为脑卒中组和非脑卒中组,记录其高血压史、年龄、平均动脉压、性别、体重指数等一般资料,采用单因素和Logistic多因素回归分析探讨脑卒中的危险因素;根据受试者高血压病程将受试者分为无高血压组、≤20a组和20a组3个亚组;根据平均动脉压水平将受试者分为正常组、≤75mmHg组和165mmHg组3个亚组,采用分层单因素方法进行研究。结果脑卒中的发生与高血压病程(OR=2.934,P=0.001)、收缩压(OR=3.046,P=0.014)、舒张压(OR=2.384,P=0.000)、平均动脉压(OR=1.879,P=4.273),年龄(OR=1.352,P=0.001),性别(OR=5.934,P=0.023)显著相关;高血压病程与脑卒中的分析中,患者的高血压史越长,发生脑卒中的几率越大(P0.05);平均动脉压水平与脑卒中的分析中,患者的平均动脉压越高,发生脑卒中的几率越大(P0.05)。结论高血压病程、收缩压、舒张压、平均动脉压、年龄、性别是发生脑卒中的危险因素;高血压病程越长、平均动脉压越大,发生脑卒中的几率越大,需临床关注。     

平均动脉压与脑出血预后的相关性分析

目的 研究平均动脉压与脑出血预后的关系.方法 对40例脑出血病人的平均动脉压进行监测,按四分位界数划分不同的范围,并与相应的神经功能恢复情况相比较,得出结果.结果 平均动脉压在前3个四分位数范围内的患者预后相对良好,相应神经功能恢复评分分别为72%、65%、60%,这与第4个四分位数(MAP,145mmHg)患者的神经功能恢复(33%)有显著差异(P＜0.01),同时观察到患者的意识状态与MAP有重要关系,意识不清者平均动脉压(139.4±4.5)mmHg,显著高于意识清楚者(130.6±19.5)mmHg.结论 脑出血病人预后与平均动脉压有关.但影响平均动脉压的主要因素是高血压和年龄,其中年龄与其呈负相关,无论意识状态如何,平均动脉压越高(＞144mmHg),其预后越差.     

高血压性脑出血住院患者的近期预后影响因素回顾性分析

目的评价血压及其它因素对高血压性脑出血近期预后的影响.方法回顾性分析我院1185例高血压性脑出血住院患者的临床资料.分别分析不同等级水平的收缩压(SBP)、舒张压(DBP)、平均动脉压(MAP)与近期预后之间的关系.采用Logistic回归分析血压及其它因素对高血压性脑出血近期预后的作用.结果平均动脉压2级组(MAP＞145mmHg)病死率明显高于平均动脉压1级组(MAP≤145mmHg),收缩压、舒张压最高等级组(SBP≥180 mmHg、DBP≥110 mmHg)病死率均最高,经统计有显著性差异.进入Logistic回归模型的自变量有5个:平均动脉压、出血量、并发症、意识水平、年龄.结论过高血压(MAP＞145mmHg)是提示近期预后不良的危险因素,平均动脉压较收缩压、舒张压更有代表性.合并并发症、重度意识障碍、高龄亦是近期预后差的重要危险因素.     

乌拉地尔强化降压治疗对高血压性脑出血患者血肿扩大的影响

目的 探讨乌拉地尔强化降压治疗对高血压性脑出血患者血肿扩大的影响.方法 将146例高血压性脑出血患者随机分为强化降压组(强化组,75例,微量泵静脉注射乌拉地尔,平均动脉压目标值为110 mmHg)和常规降压组(对照组,71例,口服卡托普利,平均动脉压目标值为130 mmHg).观察治疗后两组血肿体积、血肿扩大率、美国国立卫生研究院卒中量表(NIHSS)评分,以及死亡率和药物不良反应的情况.结果 治疗24 h后强化组血肿平均体积[(11.9±9.5)ml]、血肿扩大率(14.7%,11例)及NIHSS评分[(7.2±5.0)分]与对照组[(13.2±9.9)ml、(31.0%,22例)、(8.9±6.8)分]比较,差异有统计学意义(均P＜0.05).发病30 d后强化组NIHSS评分[(4.6±3.4)分]显著低于对照组[(5.7±4.1)分](P＜0.01);死亡率(5.3%)较对照组(9.9%)下降,但差异无统计学意义;两组不良反应差异无统计学意义.结论 乌拉地尔强化降压治疗可预防高血压性脑出血患者发生血肿扩大,并且安全可靠.     

进展性脑梗死危险因素Logistic回归分析

目的探寻引起脑梗死进展的相关危险因素。方法所选病例均为本科2004年3月～2006年5月住院的急性脑梗死患者388例,根据入院后病情演变分为进展性脑梗死组(SIP)和非进展组。观察项目包括年龄、高血压病史、糖尿病史、冠心病史、脑卒中史、高脂血症史、吸烟史、饮酒史、入院时神经功能缺损评分、入院时高血压、入院后血压降低、发热、血脂、血糖、纤维蛋白原、红细胞压积、同型半胱氨酸、颈动脉狭窄、颅内动脉狭窄。首先用单因素分析对上述观察项目(自变量)进行筛选,然后对经单因素分析有显著意义的自变量作多因素Logistic回归分析。结果388例急性脑梗死患者中符合条件的进展性脑梗死患者120例,发生率为30.93%,其中发病后24h内发生SIP32例(26.7%),48h内40例(33.3%),72h18例(15.0%),96h24例(20.0%),120h3例(2.5%),144h3例(2.5%)。进展组和非进展组之间有19个因素行χ2检验或t检验,其中有8个因素的差异有显著性,分别是糖尿病史、脑卒中史、入院后血压降低、高血糖、纤维蛋白原增高、高同型半胱氨酸、颅内动脉狭窄、颈动脉狭窄。以脑卒中是否发生进展为因变量,对经单因素分析有显著意义的自变量作多因素Logistic回归分析,回归分析显示糖尿病史、入院后血压降低、颅内动脉狭窄、高同型半胱氨酸及高血糖有显著意义,而纤维蛋白原增高、颈动脉狭窄、脑卒中史无显著性意义。结论进展性脑梗死发生率高,糖尿病史、入院后血压降低、颅内动脉狭窄、高同型半胱氨酸、高血糖是引起脑梗死进展的危险因素,寻找与脑梗死进展有密切关系的危险因子对临床降低进展性脑卒中的发生率有一定指导作用。     

中年高血压患者记忆功能障碍的临床研究

目的 探讨中年高血压患者记忆和认知功能障碍的特点及其血压参数、记忆、认知功能障碍的相关性.方法 采用临床记忆量表、简易智能精神状态量表(MMSE)、Zung抑郁自评量表对90例中年高血压患者和46例健康体检者进行测试.结果 (1)中年高血压组患者的定向力、指向记忆、联想学习、图像自由回忆、人像特点联系回忆、总量表分和记忆商(MQ)各项的等值量表分与对照组相比差异有统计学意义(P＜0.05).(2)平素最高舒张压、最高脉压与短时记忆正相关 (P＜0.05),平素最低收缩压,最低平均动脉压与语言能力负相关(P＜0.05),高血压病史与定向力负相关(P＜0.01).结论 (1)中年高血压患者存在明显的记忆和认知功能障碍,主要表现为听觉记忆、视觉记忆以及听觉和视觉记忆的结合等功能障碍.(2)高血压史、血压参数对短时记忆和认知功能有影响.     

原发性高血压脉压变化与窦性心律震荡及自主神经功能受损的作用分析

目的：探讨原发性高血压变化与窦性心律震荡（HRT ）、自主神经功能受损的关系，为心脑血管疾病的防治提供理论依据。方法随机选取我院2010-03-2013-03收入的80例原发性高血压患者作为研究对象。依据患者的脉压差值将其分为2组。A组为脉压差＞40 mmHg的患者35例，B组为脉压差＜40 mmH的患者45例。检测2组患者 HRT的震荡初始（TO）、震荡斜率（TS），与脉压进行对比，分析2组患者的 HRT情况。结果 TS＞2.5 ms/RR ，表明患者窦性心律出现减速情况。检测显示：A组35例中TO≥0、TS≤2.5 ms/RR 18例，TO＜0、TS＞2.5 ms/RR 17例；B组45例中TO≥0、TS≤2.5 ms/RR 40例，TO＜0、TS＞2.5 ms/RR 5例。经统计学分析，2组患者HRT情况具有明显差异性（χ2＝13.86，P＜0.01）。结论原发性高血压患者在脉压增大（＞40 mmHg）时，窦性心律相应减弱、消失，导致患者出现HRT异常、自主神经功能受损，更易发生心血管疾病，严重影响患者的生活质量。     

高血压脑出血术后再出血的影响因素分析

目的：研究高血压脑出血术后再出血的影响因素,为临床预防提供理论依据。方法回顾性分析2005-01-2013-01在渭南市中心医院神经外科住院经手术治疗的347例高血压脑出血患者的临床资料,其中术后再出血23例,采用病例对照研究对高血压脑出血术后再出血的影响因素进行非条件Logistic多元逐步回归分析。结果本组347例患者23例手术后24 h内发生再次出血,发生率6.63％（23/347）;单因素分析显示,年龄≥60岁、合并糖尿病、入院时GCS评分较低、口服阿司匹林、入院时舒张压＞90 mmHg、凝血异常、血肿量＞60 mL、中线结构移位和手术持续时间与术后再出血有相关性（P＜0.05）;多因素Logistic回归分析发现入院时舒张压＞90 mmHg（OR＝6.371）、凝血功能异常（OR＝21.832）和血肿量＞60 mL （OR＝28.548）是高血压脑出血术后再出血的危险因素（P＜0.05）。结论高血压脑出血术后再出血的发生率较高,入院时舒张压＞90 mmHg、凝血功能异常和血肿量＞60 mL是再出血的独立危险因素,积极处理以上危险因素对预防术后再出血至关重要。     

社区人群高血压管理及其效果分析

目的 探讨社区高血压人群管理及其效果。方法 对干预社区35岁以上人群进行高血压普查，然后对检出的确诊高血压和临界高血压患者进行为期3年的综合干预管理。结果 3年确诊高血压管理率平均为81．5％，血压达160／95mmHg以下的控制率为45．8％；3年临界高血压管理率平均为90．3％，160／95mmHg以下的控制率为75．7％；管理率随被管理对象的年龄增大而升高，但是，控制率以45岁年龄组最高，以后随年龄增高而下降。确诊高血压随访组的平均收缩压(MSBP)3年内下降了13．6mmHg，平均每年下降4．6mmHg；平均舒张压(MDBP)3年内下降了7．2mmHg，平均每年下降2．4mmHg;高血压随访组3年内心脑血管病发病率下降了46．7％，死亡率下降52．2％。结论 社区高血压人群管理是降低心脑血管病的发生和死亡的重要途径，而且是切实有效的。     

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.     

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.     

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.     

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.     

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.     

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.