舒芬太尼靶控输注用于神经外科肿瘤手术的疗效观察

目的探讨舒芬太尼靶控输注用于神经外科肿瘤手术麻醉中血流动力学变化和术后清醒的优缺点。方法 40例择期行开脑神经外科手术患者,随机分为2组,每组20例。I组采用芬太尼负荷量静注后间断静注给药方式,II组采用舒芬太尼靶控输注诱导及维持给药方式,2组患者术中全部采用丙泊酚复合(舒)芬太尼全凭静脉麻醉。术中根据血压、心率、体动及脑电双频指数(BIS)调整麻醉用量。观察记录麻醉诱导前(T0)、插管后5min(T1)、切皮(T2)、开颅骨(T3)、拔管后(T4)的SBP、DBP、HR,记录停药后患者自主呼吸恢复时间,呼之睁眼时间,拔管时间及拔管后10min、20min、30min的OAA/S(警觉/镇静评分)值。结果术中2组患者的BIS值均明显降低,维持40～60范围,2组比较差异无统计学意义(P>0.05)。各时点MAP、HR较平稳,出现明显波动,差异有统计学意义(P<0.05)。与I组比较,Ⅱ组苏醒时间及拔管时间明显降低(P<0.05),拔管后即刻OAAS评分升高,拔管后烦躁及恶心呕吐数减少(P<0.05)。结论舒芬太尼复合异丙酚把控输注静脉麻醉用于神经外科手术血流动力学稳定,苏醒期短,术后麻醉并发症少,能够取代芬太尼应用于神经外科麻醉。     

舒芬太尼与瑞芬太尼用于颅内肿瘤患者全麻诱导的比较

目的比较舒芬太尼与瑞芬太尼靶控输注（TCI）在全麻诱导期对神经外科患者血流动力学影响的差异，为临床合理用药提供支持。方法60例拟行开颅肿瘤切除术的患者，分为舒芬太尼与瑞芬太尼组（n=30）。分别接受舒芬太尼TCI（血浆靶浓度0．53ng／ml）和瑞芬太尼TCI（血浆靶浓度5．3ng／ml）诱导，均复合丙泊酚TCI和维库溴铵。比较两组患者血流动力学各参数和脑电双频指数（BIS）值的变化。结果舒芬太尼或瑞芬太尼TCI在复合异丙酚与维库溴铵行全麻诱导时，具有相似的血流动力学效应，瑞芬太尼所致血流动力学抑制较强，而舒芬太尼（血浆靶浓度0．53ng／ml）抑制气管插管所致的血压升高效果更好。两组患者BIS值无显著差异。结论就神经外科患者全麻诱导插管期的血流动力学稳定性而言，舒芬太尼优于瑞芬太尼。     

丙泊酚复合瑞芬太尼靶控输注在神经外科手术中的应用

目的探讨丙泊酚复合瑞芬太尼靶控输注全静脉麻醉在神经外科手术中应用的临床意义。方法对66例神经外科择期手术病人采用丙泊酚复合瑞芬太尼靶控输注全静脉麻醉。丙泊酚、瑞芬太尼靶浓度分别为2￣4m g/L和2￣5μg/L,间断追加维库溴胺。记录围麻醉期血流动力学、麻醉药用量以及麻醉后恢复情况。结果麻醉诱导后病人收缩压、舒张压均显著性降低(P<0.05),心率减慢(P<0.05),气管插管、切皮前后无明显改变,手术结束后睁眼时心率明显增快(P<0.05),麻醉恢复时病人苏醒较快,自觉舒适,无呼吸再抑制现象。结论丙泊酚复合瑞芬太尼靶控输注,麻醉诱导迅速,维持平稳,停药后清醒快,对气管导管耐受性好,适用于神经外科手术。     

靶控输注瑞芬太尼、丙泊酚置入喉罩静脉全麻在手腕部神经损伤修复术中的应用

目的比较靶控输注瑞芬太尼、丙泊酚置入喉罩静脉全麻与丙泊酚、芬太尼全凭静脉麻醉的效果及不良反应。方法80例手腕部神经损伤修复术病人,随机分为2组,每组40例:A组(靶控输注瑞芬太尼、丙泊酚全凭静脉麻醉组)、B组(芬太尼、丙泊酚全凭静脉麻醉组)。诱导:A组瑞芬太尼2.5μg/ml 丙泊酚3.0μg/ml,B组芬太尼3μg/kg,丙泊酚2mg/kg,诱导后均置入喉罩。术中维持:A、B组均靶控输注丙泊酚(效应部位浓度3μg/ml),分别采用复合靶控瑞芬太尼和间断静注芬太尼维持麻醉。记录各组麻醉前(T0)、诱导后(T1)、置入喉罩后(T2)、拔除喉罩(T3)各时点血压、心率变化,记录手术时间、睁眼时间、定向力恢复时间。结果2组诱导时间(A>B)、术毕睁眼时间(A>B)、定向力恢复时间(A>B)均有显著性差异(P<0.05),B组患者诱导后心率明显低于A组;A组T1、T2、T3时收缩压明显低于B组,均有显著性差异。结论靶控输注瑞芬太尼、丙泊酚置入喉罩静脉全麻可以安全有效地用于手腕部神经损伤修复术,术中患者生命体征稳定,术后苏醒迅速,是较理想的麻醉方式。     

丙泊酚靶控输注复合舒芬太尼在脑胶质瘤切除术中的应用

目的探讨不同剂量舒芬太尼复合丙泊酚靶控输注麻醉对脑胶质瘤切除术患者镇痛及神经损伤的影响。方法将75例择期脑胶质瘤切除术患者,随机数字表简单随机分组为A组(n=37)和B组(n=38);2组均采用相同的麻醉诱导(丙泊酚+舒芬太尼+罗库溴铵),麻醉诱导后,舒芬太尼靶浓度A组为0.1 ng/mL,B组为0.25 ng/mL,麻醉维持采用舒芬太尼复合丙泊酚靶控输注。记录患者围术期麻醉药物用量、术后补救镇痛及不良反应情况,分别于麻醉诱导前(T_0)、手术结束时刻(T_1)、术后1 h(T_2)、术后12 h(T_3)、术后24 h(T_4)采用酶联免疫吸附法测定患者血清S-100β蛋白(S100β)、神经元特异性烯醇化酶(NSE)水平。结果丙泊酚及舒芬太尼用量比较差异无统计学意义(P0.05);而B组术后补救镇痛率明显低于A组(15.79%vs 48.65%,P0.05)。T_0时刻,2组血清S100β、NSE水平比较差异无统计学意义(P0.05);而在T_1、T_2、T_3、T_4时刻,B组S100β、NSE水平均明显低于A组(P0.05)。2组术后不良反应发生率比较差异无统计学意义(P0.05)。结论与0.1 ng/mL靶浓度相比,舒芬太尼靶浓度0.25ng/mL复合丙泊酚靶控输注麻醉能够提高镇痛效果,并减轻患者神经损伤,且不增加不良反应。     

舒芬太尼复合丙泊酚全凭静脉麻醉在神经外科手术中的应用

目的观察舒芬太尼复合丙泊酚全凭静脉麻醉在神经外科手术中的临床效果。方法选取2012-03-2013-03在我院神将外科进行手术的患者72例,ASA分级Ⅰ~Ⅱ级。阿托品、苯巴比妥钠于术前1h分别常规肌内注射0.5mg、0.1g,麻醉诱导先后静脉输注丙泊酚1.5mg/kg、琥珀胆碱1.5mg/kg、舒芬太尼0.4g/kg,行气管插管后辅助机械通气,静脉注射维库溴铵6mg。术中给予舒芬太尼0.2g/kg,丙泊酚6mg/kg进行麻醉维持。观察患者不同时点血流动力学指标平均动脉压(mean arterial pressure,MAP)和心率(Heart rate,HR)的变化情况。结果与诱导前相比,患者的MAP在诱导后、气管插管后、头架固定时、硬脑膜关闭时及呼吸恢复后均降低,差异有统计学意义(P0.05)。诱导后HR降低,硬脑膜关闭时、呼吸恢复后及拔管后与诱导前相比,HR升高,差异均有统计学意义(P0.05)。其他时间点其MAP、HR差异无统计学意义(P0.05)。结论舒芬太尼复合丙泊酚全凭静脉麻醉镇痛作用强,药效持久,患者术中血流动力学指标稳定,意识恢复快,术后并发症少,是神经外科手术中理想的全凭静脉麻醉方法,值得推广应用。     

丙泊酚和咪达唑仑靶控镇静在颅内动脉瘤介入治疗中的对比研究

目的研究丙泊酚和咪达唑仑靶控输注清醒镇静用于颅内动脉瘤介入治疗的可行性。方法40例Hunt-Hess 0-Ⅱ级的颅内动脉瘤患者,随机分为丙泊酚组（P组）和咪达唑仑组（M组）,每组20例。术中分别采用丙泊酚和咪达唑仑实施靶控输注观察清醒镇静。记录清醒镇静评价（OAA／S）评分不同时相应的MAP、HR、SpO2和脑电双频谱指数（BIS）,以及两种药物的靶浓度（Ct）和效应室浓度（Ce）。结果随着OAA／S评分下降,MAP、HR和SpO2均明显下降（P〈0．05）;随着Ct、Ce的增加,镇静逐渐加深,OAA／S评分降低,BIS明显下降（P〈0．05）;P组镇静诱导时间和苏醒时间均短于M组（P〈0．05）。结论丙泊酚和咪达唑仑TCI清醒镇静均可用于颅内动脉瘤介入治疗,但丙泊酚安全性更高,患者合作程度更高。     

靶控输注舒芬太尼和维库溴铵静脉麻醉用于神经外科手术对比分析

目的：对比靶控输注舒芬太尼和维库溴铵静脉麻醉用于神经外科手术的麻醉效果。方法选取2012-01-2013-12我院收治并接受神经外科择期手术的患者46例，随机等分为S组与V组，分别采用舒芬太尼靶控麻醉和维库溴铵静脉麻醉，对麻醉效果及并发症情况进行评估。结果 S组与V组麻醉前后 HR、CVP、SBP及DBP均明显降低（P＜0.05）。与V组比较，S组拔管时间明显缩短，VAS评分明显提高，并发症发生率明显降低。结论在神经外科手术中，舒芬太尼靶控麻醉较维库溴铵静脉麻醉具有更佳麻醉效果和较少的并发症，适合临床应用。     

镇静深度对幕上胶质瘤术中局部脑氧饱和度监测的影响

目的观察幕上胶质瘤手术中麻醉诱导和维持阶段镇静深度改变对患者局部脑氧饱和度的影响。方法共30例美国麻醉医师协会病情分级Ⅰ～Ⅱ级、择期行幕上胶质瘤切除术的患者,以罗库溴铵、舒芬太尼以及靶控输注丙泊酚进行麻醉诱导,气管插管后全凭静脉麻醉分别以丙泊酚血浆浓度2.80～3.20μg/ml和瑞芬太尼0.10～0.20μg/(kg.min)维持麻醉,手术前连续监测并记录30组脑电双频指数、局部脑氧饱和度、平均动脉血、心率等各项监测指标直至手术开始。结果麻醉诱导过程中,随着镇静程度的加深,脑电双频指数逐渐下降,相应局部脑氧饱和度也随之出现变化,且二者之间呈负相关(r=0.803,P=0.001);而麻醉维持阶段,脑电双频指数与局部脑氧饱和度无关(r=0.147,P=0.396)。结论在全凭静脉麻醉下施行幕上胶质瘤切除术,局部脑氧饱和度监测能够准确地反映镇静深度对脑氧供需平衡的影响。     

靶控输注瑞芬太尼在颅骨钻孔引流术中的应用

目的分析对比靶控输注瑞芬太尼全麻与芬太尼全凭静脉麻醉的效果与不良反应。方法 60例颅骨钻孔引流术病人,随机分为2组,每组30例:A组(静脉注射咪达唑仑、靶控输注瑞芬太尼),B组(静脉注射咪达唑仑、芬太尼全凭静脉麻醉),术中维持:2组均静脉推注咪达唑仑,分别采用靶控瑞芬太尼和间断静脉推注芬太尼维持麻醉,记录诱导时间、手术时间、睁眼时间、定向力恢复时间。结果 2组诱导时间、定向力恢复时间、睁眼时间差异均有统计学意义(P<0.05)。结论根据监测数据个体化地调整瑞芬太尼的靶浓度,靶控输注瑞芬太尼可以安全有效地用于颅骨钻孔引流术,术中各项生命体征平稳,术后迅速苏醒,是理想的麻醉方法。     

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.     

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.     

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.     

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.     

Pediatric Epilepsy Surgery

Summary: The use of implantable arrays of epidural electrodes has made it possible to carry out extraoperative electrocorticography (ECoG) and functional localization in the awake child. This has permitted cortical excisions that are determined by criteria similar to those obtained during surgical procedures performed under local anesthesia in adults. In addition, the method also permits simultaneous ECoG and video monitoring during the child's symptomatic seizures, providing additional important localizing information that is impractical to obtain in operations under local anesthesia. We report our experience with 75 children, ages 5 months to 15 years, whom we have managed with epidural electrode arrays. The method of extraoperative ECoG is described and illustrative cases are presented to demonstrate its feasibility and utility in children. In addition, we call attention to gliomas as a common cause of chronic focal seizures in children. Of 49 children undergoing resection and followed for from 1 to 14 years (mean of 5.8 years), 32 (65%) are either seizure free or have had a significant reduction in seizure frequency that has unambiguously improved their quality of life. The results are analyzed further by relating the surgical outcome to each of the pathologic entities that caused the seizures. This analysis reveals the variety of neurological conditions that commonly cause intractable focal seizure disorder in children and distinguishes those pathologic entities in which the seizure disorder is apt to respond to surgical intervention from those that will not.     

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.