80岁以上高龄脑出血急性期患者的临床特点

目的探讨80岁以上高龄脑出血急性期患者的临床特点。方法回顾分析42例80岁以上(高龄组)和同期住院的84例50～70岁(对照组)脑出血急性期患者的一般情况、危险因素、临床表现、CT检查结果、并发症和治疗结果,并将2组资料进行统计学分析。结果与对照组相比,高龄组患者女性比例上升,较少合并高血压、吸烟等危险因素;出血部位也以基底节多见,但比例下降,而脑叶出血比例明显增加,为第二好发部位;病因仍以高血压性脑出血为主,但比例明显降低;发病时头痛症状较少,神经功能损害较重,较多出现脑疝和继发肺部感染,住院期间病死率和致残率较高。多变量Logistic分析显示女性、脑叶出血为高龄脑出血独立正相关因素,高血压性脑出血、发病早期头痛症状和入院时神经功能评分(SSS)为独立负相关因素。结论80岁以上高龄脑出血急性期患者具有一些独特的临床规律,采取相应的措施将有助于提高诊治水平。     

脑出血后癫痫发作患者临床特点分析

目的 分析脑出血急性期伴癫痫发作患者的临床特征。 方法 本研究为回顾性研究，纳入2009-2018年住院的既往无癫痫病史的自发脑出血（发病14 d内） 患者。根据脑出血急性期是否伴癫痫发作分为脑出血后癫痫发作组和脑出血后无癫痫发作组。比较 两组的一般资料及合并高血压、糖尿病、高脂血症、肺部感染、认知功能障碍等疾病的特点，同时分 析脑出血后癫痫发作患者的出血部位、侧别、病因等临床特点。 结果 共入组2836例脑出血患者，其中脑出血后伴发癫痫发作者106例，无癫痫发作者2730例。与 脑出血后无癫痫发作组患者相比，脑出血后癫痫发作患者年龄较小[（50±17）岁 vs（55±15）岁， P <0.001]，合并高血压者比例较低（60.4％ vs 86.9％，P <0.001），合并肺部感染比例较高（42.5% vs 28.5%，P =0.003）。进一步分析脑出血后癫痫发作组脑出血特点，发现脑叶出血比例较高 （57.3%），且非高血压性脑出血比例较高（59.0%）。 结论 与脑出血后无癫痫发作患者比较，脑出血后癫痫发作患者年龄较小，合并合并高血压的比 例低，住院期间肺部感染比例高；脑出血后癫痫发作患者出血多位于脑叶，多为非高血压性脑出血。     

不同部位脑出血的危险因素临床研究

目的探究不用部位脑出血的危险因素。方法选择2012-01—2014-12在我院接受治疗的脑出血患者175例为观察组。依据CT检查结果分为基底节出血58例(A组)、丘脑出血62例(B组)和其他脑叶出血55例(C组)。再随机选择同期在我院接受体检的健康志愿者70例为对照组。对比2组基本资料,并分别进行Logistics回归分析得到相应的危险因素。结果通过Logistic回归性分析,发现不同部位脑出血危险因素为:基底节脑出血的危险因素是年龄、饮酒、吸烟、高血压、SBP、DBP、TC以及HDL;丘脑部位的危险因素是饮酒、吸烟、高血压、SBP、DBP以及HDL;脑叶部位的危险因素是饮酒、吸烟、SBP、DBP以及TC。结论不同部位脑出血危险因素有所不同,主要是吸烟、饮酒及血压偏高。临床上需根据危险因素进行相应的预防,减少脑出血给患者带来的伤害。     

90例青年人脑出血病因和危险因素分析

目的探讨青年人脑出血的病因和危险因素。方法选择90例15～44岁的脑出血患者，分析其发病原因、出血部位和危险因素。结果病因为高血压病32例，动静脉畸形13例，白血病5例，海绵状血管瘤4例，动脉瘤3例，Moyamoya病3例，脑静脉血栓形成3例，脑肿瘤3例，其他3例，原因不明21例；出血部位分别是基底节出血32例，脑叶出血24例，其他部位出血34例；最常见的危险因素是高血压病（35．6％）和高甘油三酯血症（33．8％）。结论高血压病和脑血管畸形是青年人脑出血的常见病因，出血部位有助于病因诊断；高血压病、高脂血症是常见危险因素。     

中年男性脑出血患者发病因素与预后的相关性分析

目的分析中年男性脑出血患者发病因素与预后的相关性。方法回顾性分析我院2011-04—2014-04收治的280例中青年男性脑出血患者的临床资料,据年龄将其分为青年组(年龄≤44岁,n=110)与中年组(年龄45~59岁,n=170),分析其一般资料,总结发病相关危险因素,比较2组住院病死率及随访1a病死率。结果单因素分析显示,卒中史、糖尿病史、高血压史、血脂异常史、血糖及NIHSS评分为中青年脑出血发病的相关危险因素(P0.05);中年组脑出血部位多分布于基底节区、丘脑及脑叶,但青年组脑叶及脑室出血率高于中年组(P0.05),而中年组基底节区脑出血率高于青年组(P0.05);中年组住院期间病死率11.76%,1a为37.06%,均高于青年组(P0.05);年龄、血糖、NIHSS评分则为影响其预后的独立危险因素(P0.05)。结论入院时血糖显著上升且神经缺损症状较明显的中年男性脑出血患者,其不良结局发生风险更大。     

脑梗死患者微出血危险因素分析

目的探讨脑梗死急性期患者的脑微出血(cerebral microbleeds,CMBs)的危险因素。方法连续搜集2014年1月至2016年12月于福建医科大学附属第一医院神经内科住院的脑梗死急性期患者255例。根据脑微出血的部位和数目进行分组:幕下CMBs无或轻度组/中重度组、皮质CMBs无或轻度组/中重度组、深部CMBs无或轻度组/中重度组,比较不同部位各亚组之间估算的肾小球滤过率(estimated glomerular filtration rate,eGFR)水平及常见动脉硬化危险因素等的差异,并行多因素回归分析。结果共有140例患者(54.9%)存在CMBs。在幕下组中,中重度CMBs患者伴低eGFR水平的比例较无/轻度CMBs患者高(P=0.024)。低eGFR水平(OR=3.874,95%CI:1.261～11.901,P=0.018)、高血压病程(OR=2.128,95%CI:1.004～4.510,P=0.049)是幕下中重度CMBs的独立危险因素。结论肾功能不全、长高血压病程是脑梗死患者发生幕下中重度微出血的危险因素。     

不同性别青年脑出血临床分析

回顾分析近5年不同性别青年脑出血患者临床资料,男性60例、女性28例,男女比例约为2.14∶1。诸多危险因素中,男性吸烟（35%对0,P=0.000）、饮酒（28.33%对0,P=0.002）比例高于女性,女性高脂血症比例高于男性（10.71%对0,P=0.030）。男性脑出血病因以高血压居多（40%对14.29%,P=0.016）、女性以脑血管畸形为主（50%对23.33%,P=0.012）,男性脑出血好发部位主要位于基底节（35%对14.29%,P=0.045）、女性以脑叶为主（67.86%对40%,P=0.015）。提示不同性别青年脑出血在危险因素、出血部位、病因方面均存在差异。     

托吡酯治疗成人部分性癫痫发作的疗效分析

目的 探讨脑出血急性期癫痫发作的致痫因素及预后，方法 研究分析我院近期住院76例脑出血中27例急性期产切癫痫的各种致痫因素。癫痫发生率及病死率。结果 脑出血的发病初期癫痫发作发生率高，脑叶出血癫痫发生率高于基底节出血及小脑出血，脑出血急性期并发癫痫死亡率明显高于无癫痫者。结论 脑出血急性期癫痫发生率与脑出血部位，脑损伤时期密切相关。癫痫发作常使脑出血病情加重，是脑出血急性期致死的重要因素之一。     

肝硬化并发脑出血与高血压脑出血的对比研究

【摘要】 目的   探讨肝硬化并发脑出血与高血压脑出血临床特点的区别。 方法  比较首都医科大学附属北京地坛医院收治的36例肝硬化并发脑出血患者与同期我院收治的52例高血压脑出血患者出血量、出血部位及临床特点。 结果  本研究中肝硬化并发脑出血平均出血量低于高血压脑出血平均出血量（P=0.038）。两组患者脑出血部位有显著差异（P<0.001）,肝硬化并发脑出血出血部位以脑叶（44.44%）为主,而高血压脑出血多位于基底节区（80.77%）。肝硬化脑出血多部位出血者占16.67%,而本组高血压脑出血中无多部位出血,两组有显著差异（P<0.001）。 结论  与高血压脑出血相比,肝硬化并发脑出血出血量较少,部位以脑叶多见,且亦多发。        

急性脑梗死患者脑微出血与胱抑素C的相关性研究

目的探讨急性期脑梗死患者脑微出血与胱抑素C(cystatin C,Cys C)的关系。方法收集于我院2018年～2019年住院的75例急性期脑梗死患者的资料。通过核磁SWI序列检测到32例脑微出血,43例无脑微出血。所有均测定血清Cys C的水平。结果与无脑微出血组对比,脑微出血组血清Cys C水平显着升高,高于无脑微出血组,且差异具有统计学意义(P <0. 05)。结论急性脑梗死患者中年龄、高血压、Cys C水平是脑微出血的危险因素,且Cys C是急性脑梗死患者脑微出血的独立危险因素。     

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.     

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.     

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.     

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.     

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.     

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.