早期血清中高敏C-反应蛋白含量水平与急性脑梗死患者脑水肿严重程度的关系

目的 探讨早期血清中高敏C-反应蛋白(HS-CRP)不同含量水平与急性脑梗死(ACI)患者脑水肿严重程度的关系.方法 采用微粒化增强免疫固定试验测定152例ACI者人院第2天血清HS-CRP含量水平,并与30例健康人(对照组)作对照.同时观察人院第2天血清中HS-CRP不同含量水平者人院第1、3、5、7天双侧大脑半球脑电阻抗扰动系数.结果 ACI早期血清中HS-CRP含量水平明显高于对照组(P＜0.01);入院第2天血清中HS-CRP不同含量水平第1天各组间患侧、健侧电阻抗扰动系数比较无明显差异(P＜0.05),人院第3天较第1天患侧、健侧电阻抗扰动系数均明显升高(P＜0.05),P＜0.01).但HS-CRP含量水平越高,患侧、健侧电阻抗扰动系数升高越明显(P＜0.05);第7天较第3天患侧电阻抗扰动系数均明显降低(P＜0.01),但HS-CRP含量水平越低,患侧电阻抗扰动系数降低越明显(P＜0.01).结论 ACI患者早期血清中HS-CRP含量水平明显升高.其早期含量水平越高,脑水肿形成后越严重;含量水平越低,脑水肿形成后越轻,且消退越明显.     

脑出血微创血肿清除术中的无创脑水肿动态监护

目的观察脑出血患者保守治疗或微创血肿清除术治疗前后无创脑水肿动态监护仪综合扰动系数的变化,并探讨微创血肿清除手术对脑出血患者脑水肿的影响以及无创脑水肿动态监护仪监测对脑出血治疗的指导作用.方法将20例高血压性脑出血患者随机分为2组,微创血肿清除手术组(微创组):10例脑出血患者于入院6～24 h内接受简易立体定向微创血肿清除术治疗;对照组:10例脑出血患者接受内科保守治疗,所有病例均于入院后1、3、5、7 d采用无创脑水肿动态监护仪动态检测综合扰动系数.结果无论是对照组还是微创组入院后即刻检查均是患侧综合扰动系数低于健侧,随着病程推移对照组出现患侧扰动系数升高并超过健侧,3 d时达到高峰,并持续7 d以上;随着病程推移微创组出现3 d时患侧高于健侧,5 d时两侧接近,7 d时两侧基本正常;病程第3、5、7 d时2组综合扰动系数比较差异有显著性意义(P＜0.001).结论脑出血患者综合扰动系数呈不对称性改变,且随病程推移呈现动态变化,并反映了水肿形成过程,微创血肿清除术能有效清除血肿,可显著性改善脑出血后的脑水肿形成,无创脑水肿动态监护仪可动态评估患者脑水肿演变过程,对再出血的诊断及治疗有一定的指导意义.     

铁蛋白在高血压脑出血后血肿周围脑水肿中的作用及机制研究

目的探讨血清铁蛋白与高血压脑出血后血肿周围脑水肿的关系,并分析其在血肿周围脑水肿发生中的作用。方法采集2012-05—2013-11于我院住院治疗的38例高血压脑出血患者的临床资料和实验室数据,所有患者均在入院时及入院3~4d后行血清铁蛋白及头颅CT检查,计算入院时及入院3~4d后血肿体积、脑水肿总体积及经校正后的相对水肿体积,采用Spearman相关分析相对血肿周围脑水肿体积与血清铁蛋白的关系。结果与入院当天比较,入院第3~4天后血肿体积增加19%,但差异无统计学意义(P0.05);脑水肿体积增大71%,差异有统计学意义(P0.05)。血肿周围脑水肿体积与血肿体积的比值即相对水肿体积增加1.13倍。入院当天,患者血清铁蛋白水平和相对水肿大小间无明显相关性(P0.05);入院后第3~4天时相对水肿体积与血清铁蛋白呈正相关(r=0.67,P=0.006)。结论血清铁蛋白是反映高血压脑出血后血肿周围脑水肿程度的一个重要指标,其在血肿周围继发性脑水肿的发生中起重要作用。     

不同术式对自发性脑出血周围水肿带的影响

目的通过比较微创脑内血肿穿刺外引流术与开颅血肿清除术对自发性基底节区脑出血周围水肿带大小的比较,为脑出血的治疗寻找较为理想的治疗方案。方法对51例自发性基底节区脑出血病人进行回顾性分析,其中26例接受微创脑内血肿外引流术,25例接受开颅手术清除血肿。将手术前后两组病人血肿周围脑水肿带体积进行比较。结果微创手术组术后7天血肿周围水肿体积小于开颅血肿清除手术组(P<0.05)。结论微创手术组对血肿周围脑组织损伤小,可作为高血压性脑出血手术治疗的首选术式。     

急性脑出血血肿体积动态变化研究

目的 研究急性脑出血血肿体积动态变化.方法 对30例急性期脑出血患者分别于起病6h以内、1d、3d、7d、14d进行头颅CT扫描,采用体视学法对脑出血血肿及周围低密度水肿灶进行测量,计算二者比值,并根据出血量将患者分为少量及中等量出血组,比较2组血肿、水肿体积及CSS评分. 结果 脑出血急性期血肿体积逐渐缩小,周围低密度水肿灶体积逐渐扩大,7～14d达高峰,差异有统计学意义(P＜0.05),血肿体积与周围低密度水肿灶体积有相关性(|r|=0.75),2组的血肿/水肿比值差异无统计学意义(P＞0.05),2组的CSS评分差异有统计学意义(P＜0.05),但2组的水肿体积与CSS评分无相关性.结论 急性脑出血后起病至3d血肿体积无明显变化,水肿体积小,3～7d后血肿开始逐渐缩小,而水肿明显扩大,14d达高峰.少量及中等量出血血肿及水肿体积变化规律相同,血肿量直接影响CSS评分,而与水肿量无明显相关性.     

急性期脑出血灶周水肿的磁共振弥散加权成像临床初步研究

目的应用磁共振弥散加权成像(DWI)探讨急性期脑出血血肿周围水肿性质及形成机制。方法对满足检查条件的连续发病2周内的44例脑出血患者进行DWI成像,测量血肿周围1cm区域和水肿区表观弥散系数(ADC)的变化情况,对水肿区相对ADC与水肿体积做相关分析。结果44例脑出血患者血肿周围均存在水肿,40例患者血肿周围ADC升高,水肿区ADC较对侧对称区域升高58．6%差异有非常显著性意义(P＜0．001),血肿周围1 cm区域较对侧对称区域ADC升高24．1%;水肿区相对ADC与绝对水肿体积和相对水肿体积呈正相关(P=0．003)。另4例患者血肿周围水肿区ADC降低。结论急性期大部分血肿周围水肿ADC升高,血管源性水肿是其主要的发生机制;少数患者血肿周围水肿ADC下降,提示细胞毒性水肿占主导地位,患者病情多危重,预后不良。     

阻塞性睡眠呼吸暂停低通气综合征与高血压性脑出血血肿周围水肿的相关性

目的 分析阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea-hypopnea syndrome,OSAHS)与高血压性脑出血血肿周围水肿的相关性.方法 收集高血压性脑出血患者144例,其中合并OSAHS患者78例.不合并OSAHS的高血压性脑出血患者66例,作为空白对照组,两组患者均接受常规脱水降颅压、降压、保护脑细胞治疗.在入院时行头CT检查并于24h内行夜间多导睡眠图(polymonography,PSG)监测.入院后24 h及第4天均复查CT,测量脑血肿体积和血肿周围水肿体积,动态观察脑血肿及血肿周围水肿变化.结果 伴或不伴OSAHS两组在年龄、性别组成、体重指数、血糖、血脂等方面差异均无统计学意义.两组患者的相对水肿体积指数(relative edema index,REI)在入院时和24 h后差异均无统计学意义；入院第4天,OSAHS组水肿体积变化指数为0.96±1.35,明显高于对照组(0.40±0.45,t=4.149,P=0.000).不同程度OSAHS患者的水肿体积及水肿变化的分析结果表明,入院时不同程度OSAHS的脑出血患者的脑水肿程度差异无统计学意义(无OSAHS组和轻、中、重组分别为1.05士0.65、0.84±0.48、1.20±0.54、1.10±0.40,F=1.061,P=0.374)；入院24h和第4天时,随着OSAHS严重程度的增加,脑出血患者的脑水肿程度增加.水肿体积变化差异性分析显示,重度OSAHS合并症的患者,水肿体积增加更明显.水肿变化指数与OSAHS程度指标呼吸暂停低通气指数呈明显正相关,Pearson相关系数为0.652(P =0.000).结论 OSAHS可加重高血压性脑出血患者的水肿恶化程度,且恶化程度与OSAHS严重程度呈正相关.     

脑出血后脑水肿程度评估及其影响因素分析

目的 应用改良方法对脑出血后脑水肿程度进行量化评估,分析影响脑水肿程度的相关因素.方法 140例出血量在10ml以上的脑出血住院患者于发病当天、发病后3d、7d和14d进行头部CT扫描,计算脑出血血肿体积及周围水肿体积,分析影响脑出血后脑水肿程度的相关因素.结果 140例入选的脑出血患者,发病当天脑出血平均体积23.87±8.2ml.随着发病时间延长,脑血肿体积逐渐缩小,脑出血后脑水肿在发病当天即可出现,发病后3d的脑水肿体积显著增高(P<0.01),增高趋势延续至发病后14d(P<0.01).应用改良方法测得的血肿体积与传统方法测量结果大致相仿,但测得的水肿体积高于传统方法测量结果(P<0.05).脑出血量大,伴发高血压、糖尿病、缺血性脑血管病、肺部感染、肾功能不全、低钠血症、占位效应的患者脑出血后脑水肿体积明显增大(P<0.01,P<0.05).结论 脑出血后脑水肿程度随着脑出血时间动态变化,改良方法对于脑水肿体积的评估更加客观与准确,脑出血量大,伴发糖尿病、缺血性脑血管病、肺部感染、肾功能不全、低钠血症、占位效应是加重脑出血后脑水肿程度的危险因素.     

SHR大鼠脑出血急性期氨氯地平血压干预和血肿周围水肿的相关性研究

目的采用自发性高血压大鼠(SHR)脑出血模型,研究脑出血后急性期血压和血肿周围水肿的相关性。方法胶原酶法制备SHR大鼠脑出血模型,出血部位为右侧基底节区。动物随机分为脑出血组、脑出血常规剂量氨氯地平降压组、脑出血强化剂量氨氯地平降压组。MRI检查并计算血肿周围水肿大小;免疫组化及荧光定量PCR法检测血肿周围水肿的AQP4表达。结果 (1)氨氯地平治疗组MRI检测值显示,脑血肿周围水肿减轻,降压组均优于未干预组,强化降压组优于常规降压组,差异有统计学意义,第3、5、7天的F值分别为16.987、35.448、37.174(P<0.05);收缩压降低幅度和血肿周围水肿体积之间有相关性,在第3、5、7天的相关系数r分别为0.83、0.89、0.83,P=0.000;舒张压降低幅度和血肿周围水肿体积之间有相关性,在第3、5、7天的相关系数r分别为0.82、0.89、0.84,P=0.000)。(2)降压组血肿周围水肿的AQP4表达下调均优于未干预组,强化降压组优于常规降压组,差异有统计学意义,第3、5、7天的F值分别为217.058、21、51.706(P<0.05)。结论 (1)氨氯地平有效降压能使脑出血血肿周围水肿缩小;(2)氨氯地平可能通过抑制AQP4表达促使血肿周围脑水肿减轻;(3)收缩压、舒张压的升高均可促使血肿周围脑水肿扩大。     

老年高血压脑出血患者血清脑钠肽的动态变化与脑水肿的关系

目的探讨高血压脑出血患者血清脑钠肽(BNP)变化与脑水肿的相关性。方法将我院神经外科收治的85例高血压脑出血患者根据是否发生脑水肿分为脑水肿组(36例)与非脑水肿组(49例),并选取同期住院高血压但未发生脑出血患者40例为对照组,比较3组患者入院6h、24h、48h、72h、96h、118h、142h、166h的BNP及脑水肿变化趋势,并分析二者间的相关性。结果术后6h、24h、48h、72h、96h、118h、142h、166h3组血浆BNP水平、电阻抗扰动系数比较差异有统计学意义(P0.05),脑水肿组除术后6h与非脑水肿组比较差异无统计学意义外,其他时间均显著高于非脑水肿组和对照组(P0.05),非脑水肿组BNP、电阻抗扰动系数在各时间点均显著高于对照组(P0.05)。脑水肿患者BNP水平与电阻抗扰动系数值有显著相关性(r=0.545,P=0.001)。结论高血压脑出血患者血BNP水平变化与脑水肿具有一定关系,通过早期检测BNP有利于采取措施防止脑水肿形成。     

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.     

Treatment Considerations in Anticonvulsant Monotherapy

Summary: The long-standing practice of polypharmacy in treating epilepsy is giving way to use of monotherapy. Monotherapy can improve seizure control as well as reduce the risk of serious idiosyncratic reactions, dose-related side effects, and complex drug interactions. Monotherapy also offers improved compliance and cost-effectiveness. The basis of monotherapy is accurate diagnosis and assessment of the patient's seizure type(s), followed by selection of a single appropriate anticonvulsant drug. Many patients currently treated with multiple anticonvulsants can be successfully converted to monotherapy with a carefully monitored program in which troublesome and redundant drugs are gradually withdrawn from the therapeutic regimen.     

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.     

Dextromethorphan: Cellular Effects Reducing Neuronal Hyperactivity

Summary: Dextromethorphan is a dextrorotary morphinan without affinity for opioid receptors, commonly used as an antitussive medication. During the past 5 years, interest in the compound and its demethylated derivative, dextrorphan, has been revived because additional neuroprotective and an-tiepileptic properties were found in in vitro studies, animal experiments, and a few clinical cases. Both morphinans are able to inhibit N -methyl-D-aspartate (NMDA) receptor channels and voltage-operated calcium and sodium channels with different potencies. The inhibition of the NMDA receptor is believed to be the predominant mechanism of action responsible for the anticonvulsant and neuroprotective properties of the compounds.