大剂量醒脑静对小儿颅脑损伤的治疗作用

目的 探讨大剂量醒脑静对小儿颅脑损伤的治疗作用。方法 按标准选取1～12岁患儿40例并随机分为受试组和对照组。受试组入院后30min内接受醒脑静2ml/kg,此后,每12h接受静滴醒脑静2ml/kg,共计5d;对照组不用此药,5d后查血清内皮素(ET)和一氧化氮(NO)的含量。2周后测格拉斯哥昏迷评分(GCS),6个月后测格拉斯哥预后分级(GOS),然后行统计学分析。结果 受试组与对照组的ET分别为(53.48±13.87)ng/L和(71.13±12.37)ng/L;NO分别为(56.10±23)μmol/ L和(39.16±13.12)μmol/L;GOS分别为3.8±1.4和3.6±1.6 ;两组间ET和GCS的差异有显著意义(P<0.01和P<0.05),而GOS差异无统计学意义(P>0.05)。结论 大剂量醒脑静治疗小儿脑外伤近期疗效显著。     

扩容疗法应用于动脉瘤术后脑血管痉挛的效果观察

目的观察扩容疗法应用于动脉瘤术后脑血管痉挛的效果。方法将106例动脉瘤术后脑血管痉挛患者知情同意后分为观察组和对照组各53例。对照组给予尼莫地平治疗,观察组在此基础上给予胶体溶液静脉输注扩容治疗。对比2组经颅多普勒超声(TCD)检查结果、CT检查结果、GCS评分、血流动力学指标变化和不良反应发生率。结果观察组治疗后7d和14d的TCD值显著低于对照组(P0.01)。2组Fisher评分差异无统计学意义(P0.05)。观察组治疗后7d和14d的GCS评分显著高于对照组(P0.01)。观察组治疗后、灌注后的收缩压和舒张压显著低于对照组(P0.05)。2组不良反应发生率差异无统计学意义(P0.05)。结论扩容疗法应用于动脉瘤术后脑血管痉挛可有效改善患者脑部供血,但会降低血压,临床治疗中应予以重视。     

依达拉奉防治颅内动脉瘤术后迟发性脑血管痉挛的疗效观察

目的观察依达拉奉治疗颅内动脉瘤术后迟发性脑血管痉挛的疗效。方法60例脑动脉瘤术后患者随机分为治疗组和对照组,每组各30例。治疗组在常规治疗基础上加用依达拉奉注射液30mg,静滴,每日2次,14d后进行疗效评价。结果治疗组发生迟发性脑血管痉挛(DCVS)者仅2例,其发生率明显低于对照组(P<0.05);治疗组总有效率93.3%,而对照组为73.3%,两组比较有显著差异(P<0.05)。治疗组防治脑动脉瘤术后迟发性脑血管痉挛效果明显优于对照组。结论依达拉奉作为一种新型羟自由基清除剂,可以作为防治颅内动脉瘤术后迟发性脑血管痉挛有效的药物。     

腰椎穿刺脑脊液置换对不同H-H分级蛛网膜下腔出血预后的影响

目的 探讨腰椎穿刺脑脊液置换对不同H-H分级动脉瘤性蛛网膜下腔出血(aneurysmal subarachnoid hemorrhage, aSAH)患者迟发性脑血管痉挛发生率及入院90 d预后的影响。方法 回顾性纳入接受颅内动脉瘤栓塞术的aSAH患者,所有患者均与入院3 d内行脑动脉瘤弹簧圈栓塞; 依据H-H分级是否≥Ⅲ级将患者分类后分别对这两类患者按照治疗方案分为脑脊液置换组和非脑脊液置换组。Ⅰ和Ⅱ级aSAH患者中非脑脊液置换组42例,脑脊液置换组46例; ≥Ⅲ级患者非脑脊液置换组53例,脑脊液置换组56例,比较脑脊液检查、颅内感染发生率、迟发性脑血管痉挛发生率、住院时间及入院90 d预后。结果 Ⅰ和Ⅱ级aSAH患者非脑脊液置换组与脑脊液置换组比较,迟发性脑血管痉挛发生率、住院时间及入院90 d预后均无明显差异(P均>0.05); ≥Ⅲ级患者迟发性脑血管痉挛发生率非脑脊液置换组(28.3%)明显高于脑脊液置换组(10.7%)χ²=5.415,P=0.020),且住院时间明显延长(t=2.231,P=0.045),预后较差χ²=4.380,P=0.036)。两类患者中非脑脊液置换组与脑脊液置换组颅内感染率均未见明显增加,且无明显差异(P>0.05)。结论 腰椎穿刺脑脊液置换能够减少≥Ⅲ级蛛网膜下腔出血患者迟发性脑血管痉挛发生率,缩短住院时间,改善患者预后,但不能改善Ⅰ和Ⅱ级蛛网膜下腔出血患者入院90 d预后。     

Rho激酶抑制剂对动脉瘤性蛛网膜下腔出血后迟发性脑血管痉挛的疗效研究

目的 探讨Rho 激酶抑制剂对动脉瘤性蛛网膜下腔出血(aSAH)后迟发性脑血管痉挛(DCVS)的治疗效果.方法 按照是否应用Rho 激酶抑制剂对35 例自发性性蛛网膜下腔出血后发生迟发性脑血管痉挛的患者资料和治疗效果进行回顾性分析.结果 Rho 激酶抑制剂对迟发性脑血管痉挛临床症状改善率81.25%,与常规治疗组47.37%相比,具有统计学差异(P＜0.05);治疗后,Rho 激酶抑制组脑血流速度低于对照组(P＜0.05).结论 Rho 激酶抑制剂能明显缓解aSAH 后迟发性脑血管痉挛的临床症状,为神经外科防治迟发性脑血管痉挛提供了临床依据.     

电针配合尼莫地平治疗大脑中动脉瘤夹闭术后脑血管痉挛

目的探讨电针配合尼莫地平治疗大脑中动脉瘤夹闭术后脑血管痉挛的疗效。方法回顾性分析60例经显微夹闭术处理破裂大脑中动脉瘤患者,术后TCD证实不同程度脑血管痉挛,30例术后应用尼莫地平持续泵入(甲组),连用14d;30例在尼莫地平组治疗基础上加用电针疗法(乙组),选用下关、百会及风池穴。术后3d、7d及14d评估GCS评分、脑血管痉挛程度、mRS评分等。结果术后7d和14d,乙组GCS评分明显高于甲组,脑血管痉挛为轻度比例达76.7%、93.3%;术后1个月随访,乙组mRS评分好于甲组,差异均有统计学意义(P0.05);而术后3d,2组GCS评分及脑血管痉挛恢复程度差异无统计学意义(P0.05)。结论尼莫地平配合电针对大脑中动脉瘤破裂所致脑血管痉挛有一定改善作用,时间越长,效果可能越明显。     

醒脑静治疗蛛网膜下腔出血临床分析

目的探讨醒脑静治疗蛛网膜下腔出血(SAH)的方法和疗效。方法随机将50例SAH患者分为醒脑静组(25例)和对照组组(25例)。对照组应用常规药物包括尼莫地平,醒脑静组在常规药物治疗基础上加用醒脑静治疗。行经颅多普勒(TCD)动态检测大脑中动脉、颈内动脉颅外段的平均血流速度及脉动指数,评定治疗效果。结果醒脑静组的脑血管痉挛(CVS)发病率明显低于对照组(P<0.05),持续时间也明显缩短(P<0.05)。第7d及第10d时醒脑静组平均血流速度(VMCA)较对照组有明显降低(P<0.05),2组间脉动指数(PI)值无明显差异(P>0.05)。结论醒脑静可显著降低SAH患者的大脑中动脉血流速度(MCA),降低CVS发生的频率,缩短CVS持续时间,减弱CVS的强度,认为醒脑静治疗对防治CVS有显著作用。     

两种剂量纳洛酮治疗重型颅脑损伤的疗效观察

目的比较盐酸纳洛酮在治疗重型脑损伤中两种剂量的治疗效果。方法126例重型脑损伤病人随机分为甲乙两组,甲组每天给予纳洛酮0.4mg/kg体重,用平衡液500ml稀释后微泵24h持续静滴,连用3d后统一减量为4.8mg/d,连用7d后停药;乙组按同样方法给予每天0.4mg/kg体重,连用7d后停药;观察第10d GCS和GOS。结果第10d的GCS和GOS甲组分别为9.41和3.23±1.71,乙组为10.52和3.97±1.64,有显著性差异(P<0.05)。结论治疗重型脑损伤中延长大剂量纳洛酮的治疗时间可提高疗效。     

恩必普联合依达拉奉治疗脑梗死疗效观察

目的观察恩必普(NBP)联合依达拉奉治疗急性脑梗死(CI)疗效。方法入选121例CI住院患者,随机分为对照组58例及治疗组63例。对照组仅采用CI常规治疗,治疗组在常规治疗基础上加用NBP餐前口服200 mg、3次/d、21 d,依达拉奉30 mg+0.9%氯化钠注射液100 ml静点12 h 1次、14 d。治疗前后进行神经功能缺损程度评定;神经功能缺失评分采用NIHSS评分:分别在开始NBP治疗前、治疗后7、14、21 d时进行评定。结果治疗21 d后神经功能缺损程度评定,治疗组有效率为92.06%(58/63),对照组有效率为75.86%(44/58),P<0.05。治疗21 d后,NIHSS治疗组4.41±1.26分,对照组7.04±1.25分,P<0.01。结论 NBP联合依达拉奉治疗CI疗效显著。     

蛛网膜下腔出血后无迟发性脑缺血相关因素分析

目的 分析动脉瘤性蛛网膜下腔出血(aSAH)后无迟发性脑缺血(DCI)的相关因素,以期为DCI病人转出重症监护病房(ICU)提供临床依据.方法 选取2001-10 2011-06确诊的动脉瘤性蛛网膜下腔出血且入住重症监护病房患者153例,其中DCI组67例,非DCI组86例;分析蛛网膜下腔出血后无迟发性脑缺血的相关因素.结果 DCI组一般情况相比非DCI组显示:平均年龄、入院血糖＞6.1 mmol/L、后循环动脉瘤、脑室出血差异有统计学意义(P＜0.05);服用他汀类药物、GCS评分、WFNS Ⅰ～Ⅲ级、改良Fisher分级Ⅰ～Ⅱ级、TCD血管痉挛、血管造影血管痉挛差异有统计学意义(P＜0.001);单因素分析显示:年龄＞65岁,WFNS分级Ⅰ～Ⅲ级、改良Fisher分级1～2级、无颅内血肿和后交通动脉瘤与动脉瘤性蛛网膜下腔出血后无迟发性脑缺血相关(P＜0.05);多因素分析发现年龄＞65岁,WFNS Ⅰ～Ⅲ级,改良Fisher分级1～2级是未发生DCI的独立因素.结论 年龄＞65岁,WFNSⅠ～Ⅲ级和改良Fisher分级1～2级可作为病人转出ICU病房的依据.     

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.     

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.     

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.