丘脑胶质瘤X-刀治疗近期疗效分析

目的研究丘脑原发或复发性胶质瘤X-刀治疗的疗效。方法丘脑胶质瘤23例，肿瘤平均体积12．47cm^3，17例单次治疗肿瘤周边放射剂量14～21Gy，6例分次治疗放射剂量23～35Gy／6次。结果生存率6个月94．75％，1年68．54％，2年36．43％，肿瘤6个月控制率90．7％，中位复发时间9个月，中位生存期13个月。结论丘脑胶质瘤X-刀治疗可延长患者生存期，提高肿瘤局部控制率。     

立体定向X-刀加血脑屏障开放化疗治疗脑转移瘤

<正>脑转移瘤是最常见的颅内恶性肿瘤之一,随着医学影像学技术的发展及肿瘤患者生存时间的延长,肿瘤脑转移的发病率有逐年上升趋势[1]。颅内多发转移瘤及位于脑深部及重要功能区的脑转移瘤,一直是神经外科的治疗难点之一。我科1998-04-2010-09采用德国Brain LAB X-刀,加用血脑屏障开放、颈动脉灌注化疗相结合的方法治疗脑转移瘤患者102例,取得较好效果,现报告如下。1资料与方法     

X-刀治疗颅内病变(附128例临床报道)

目的:总结X-刀治疗顿内疾病的经验。方法:1994年7月～1997年3月用X-刀治疗颅内疾病128例,共134个病灶,其中脑转移瘤47例,胶质瘤28例,脑膜瘤16例,脑血管畸形19例,松果体瘤7例,其它肿瘤11例。结果:74例随访3个月～2年,其中病变消失25例(33.8％),病变缩小24例(32.4％),病变坏死7例(9.5％),病变无变化14例(18.9％),病变增大4例(5.4％)。结论:临床应用初步结果证实X-刀治疗颅内疾病短期效果较为满意,是一种治疗颅内疾病的安全和有效的手段。     

伽玛刀治疗胶质瘤的近期效果分析

目的 探讨不同级别的脑胶质瘤伽玛刀治疗后的近期效果。方法自2002年6月至2004年8月对病理诊断明确的97例脑胶质瘤患者进行了伽玛刀治疗,随访66例,其中位于颞叶10例,额叶16例,顶叶11例,枕叶6例,丘脑9例,小脑6例,脑干5例,视交叉3例,体积在3～32cm^3之间,平均10.38cm^3。29例病人伽玛刀治疗前经开颅手术,大多数肿瘤的边缘剂量为12～16Gy(6～25Gy),相应的中心剂量为25～30Gy(14～55Gy)。结果平均随访时间为8．1个月(3～24个月),经MRI或CT复查．治疗后3～6个月,28．8％肿瘤体积减小,42.4％肿瘤停止生长,21．2％肿瘤继续增大,死亡5例,占7．7％。25.8％患者肿瘤周围出现不同程度的水肿,19．7％的患者原来的瘤周水肿减轻或消失。结论伽玛刀是治疗脑胶质瘤的一种有效的方法。     

X-刀开放瘤周血脑屏障后化学治疗脑部恶性肿瘤

目的探讨X-刀联合全身化疗治疗脑部恶性肿瘤的具体方法和临床疗效。方法选择脑部恶性肿瘤病人52例,随机分为联合治疗组(n=31)和单纯X-刀治疗组(对照组,n=21)。联合治疗组在X-刀治疗3周后行多个疗程的全身盐酸尼莫司汀(ACNU)治疗;对照组仅采用X-刀治疗,比较两组治疗效果。结果①两组在X-刀治疗3周后均可观察到血脑屏障、脑肿瘤屏障开放。②60周时联合治疗组29例(93.5%)生存,对照组14例(66.7%)生存,差异有统计学意义(P<0.05)。结论采用X-刀治疗脑部恶性肿瘤,增强了化疗效果,两者联用有助于提高病人的生存率。     

经颈动脉灌注化疗治疗脑胶质瘤

目的研究脑胶质瘤术后经颈动脉灌注化疗的临床效果，探讨药物选择、给药途径及化疗时机等相关问题。方法对212例胶质瘤病人于术岳4～30d经颈动脉灌注盐酸尼莫司门2．5mg／kg，每周1次，3次为1个疗程，4～6周后行第2疗程治疗。结果显效(CR)39例，占18．8％；有效(PR)44例，占20．8％；微效(MR)59例，占27．8％；无变化(NC)61例，d／28．8％；恶化(PD)5例，占2．4％。中位生存期接近100周。结论经颈动脉灌注治疗脑胶质瘤具有疗效好、副作用小、简便、经济、病人愿意接受等诸多优点。     

脑转移瘤的X-刀治疗（附23例报告）

目的：总结我院用X-刀治疗脑转移瘤的经验。方法：以Bmin Scan Ⅱ型X-刀治疗脑转移瘤病人23例，共38个病灶。治疗计划为：病灶体积为1340±9．35cm^3，等中心数目1至3个不等，准直仪直径为10～40mm，中心剂量为22.25=3.24Gy，肿瘤边缘剂量为15.75=2.93Gy。其中17例加作了全脑放射治疗。结果：随访852±354个月，病灶经X-刀治疗后局部控制率为89．47％。病人因脑转移瘤而产生的症状均明显改善或消失，其平均生存时间为788±324个月，加作全脑放疗的平均生存时间明显较单纯X-刀治疗为长。未发现放射性水肿、坏死及自发性瘤内出血等严重的并发症。已死亡8例，死亡原因与X-刀所治疗的转移灶无关。结论：X-刀或其它立体定向放射神经外科是治疗脑转移瘤的良好方法，但应慎重选择适应证，加强术后处理．并结合其它治疗手段。     

胶质瘤伽玛刀治疗的初步结果

本报告应用γ-刀治疗48例经手术治疗、术后放疗和(或)化疗后复发的胶质瘤。其中男30例、女18例，年龄平均38岁(7～74)岁。肿瘤最大直径11.3～69．8mm,平均35mm。最大中心照射剂量22～55Gy，平均32Gy。肿瘤周边剂量11～20Gy，平均15Gy。照射的等中心点数1～15个，平均7个。随访40例，随访率83．3％，随访时间9～22个月，平均14个月。至最后一次随访时，死亡16例。3例症状好转．9例病情无加重。40例的存活时间：2～22个月，平均10．9个月。肿瘤直径小治疗效果好，而肿瘤直径大疗效不佳。     

可逆性血脑屏障开放对脑瘤化疗的临床意义

本文将20例恶性脑瘤患者分为两组。Ⅰ组:用20％甘露醇行可逆性血脑屏障(BBB)开放,继之经颈动脉灌注顺铂(CDDP);Ⅱ组:仅灌注同剂量CDDP。分别测定肿瘤及正常脑组织内 CDDP浓度。结果表明:用 20％甘露醇行可逆性BBB开放能显著增加肿瘤内药浓度,而正常脑组织内药浓度变化不明显。此技术对提高脑瘤化疗效果具有重要的临床价值。     

X-刀治疗脑转移瘤（附58例报告）

目的:总结X-刀治疗脑转移瘤临床效果。方法:我院用X-刀治疗脑转移瘤58例,共78个病灶,肿瘤周边剂量平均为19.73Gy,一般以70％～100％等剂量线覆盖肿瘤周边,28例患者配合全脑放疗。结果:随访3～26个月,CT和MRI随访47例,证实肿瘤治疗后完全消失(CR)20例(42.6％),大部分缩小(PR)8例(17.0％),部分缩小(MR)8例(17.0％),无变化(NC)6例(12.8％),增大(PG)5例(10.6％),脑水肿3例,无放射性脑坏死发生。临床随访50例,死亡36例,平均存活期12.0个月;生存14例,已平均存活9.5个月。颅外病变稳定者X-刀术后生存期比颅外病变活跃者长。对部分患者应配合全脑放疗。结论:该技术治疗脑转移瘤近期效果较为满意,是一种安全有效的方法。     

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.     

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.