伽玛刀治疗良性颅底脑膜瘤

目的探讨伽玛刀放射外科治疗良性颅底脑膜瘤中长期疗效和毒性。方法选取了1997~2002年治疗的颅底脑膜瘤患者196例,肿瘤体积平均6.2±4.9cm3,给予中心剂量平均27.9±5.9Gy,周边剂量平均12.4±1.6Gy。随访根据治疗前后的影像表现和行为评分进行评估。结果平均随访期为53.4±18.2个月(36~96个月),有完整随访资料患者178例。肿瘤的控制率为93.3%;临床表现满意度(好转和稳定)92.7%,神经症状总改善率为93.8%,并发症少且轻微。结论伽玛刀可作为颅底较大脑膜瘤开颅术后的辅助治疗,也可作为较小肿瘤或对手术禁忌患者的首选性治疗;对长期控制肿瘤复发,保证患者良好的生存质量起重要的作用。     

颅底脑膜瘤的伽玛刀治疗

目的研究伽玛刀放射外科治疗颅底脑膜瘤的效果。方法选取了1995-2000年治疗的颅底脑膜瘤患者225例,肿瘤体积平均6.0±5.2cm3,给予中心剂量平均27.5±5.2Gy,周边剂量平均12.3±1.9Gy。随访根据治疗前后的影像表现和Karnofsky行为评分进行评估。结果有完整随访资料患者189例。从总体上,肿瘤的控制率为96.8%;临床表现满意度(好转和稳定)96.3%,并发症少且轻微。结论伽玛刀可作为颅底较大脑膜瘤开颅术后的辅助治疗,也可作为较小肿瘤或对手术禁忌患者的首选性治疗;对长期控制肿瘤复发、保证患者良好的生存质量,起重要的作用。     

脑膜瘤分阶段伽玛刀放射外科治疗的策略及疗效分析

目的 探索存在手术禁忌证的体积较大或靠近重要神经结构的脑膜瘤患者的分阶段伽玛刀放射外科治疗的策略及其疗效。方法 80例脑膜瘤患者,其中61例患者接受剂量分割分阶段放射外科治疗,单次周边剂量为7～11 Gy,40%～50%的等剂量线; 19例患者接受体积分割分阶段放射外科治疗,单次周边剂量为8～14 Gy,40%～50%的等剂量线。分阶段治疗的时间间隔为3～17个月,平均(9. 1±3. 1)个月。治疗后随访时间为6～72个月,平均(36. 5±7. 2)个月。结果 所有患者均顺利完成治疗计划,未出现严重不良反应和新发神经功能障碍者。两个阶段治疗后6个月、1年、2年和3年患者的肿瘤体积分别缩小了(25. 27±19. 13)%、(24. 98±19. 82)%、(30. 49±17. 64)%和(32. 12±16. 55)%。结论 对于体积较大或邻近重要结构的脑膜瘤采用分阶段伽玛刀放射外科治疗有显著的效果和安全性;该治疗方案为存在开颅手术禁忌证的脑膜瘤患者提供了一个最佳的治疗选择。     

颅底脑膜瘤的伽玛刀治疗

目的:评估伽玛刀(γ-刀)在治疗颅底脑膜瘤中的作用。方法:采用30％～60％等剂量曲线覆盖肿瘤,平均边缘剂量13.5Gy(10～16Gy),中心剂量32 Gy(20～45Gy) 治疗顿底啮膜瘤49例结果:平均随访15个月,17例病人保持或改善了治疗前的神经功能状态,4例加重;37例病人的影像学随访,14例肿瘤体积无变化,20例缩小,3例增大,肿瘤生长控制率达92％(34/37)。结论:早期随访结果提示γ-刀是治疗颅底脑膜瘤安全有效的手段。     

颅内非听神经性神经鞘瘤的放射外科治疗临床研究

目的 回顾性分析伽玛刀放射外科对非听神经性神经鞘瘤的疗效及治疗剂量.方法 应用γ刀治疗非听神经神经鞘瘤,43例获得完全随访资料,包括24例三叉神经鞘瘤和19例颈静脉孔神经鞘瘤.以50%～80%等剂量曲线包绕靶区,肿瘤中位剂量分别为13 Gy(三叉神经鞘瘤)和15 Gy(颈静脉孔神经鞘瘤).结果 43例患者平均随访时间62个月.本组随访影像提示24例三叉神经鞘瘤患者伽玛刀治疗后肿瘤基本消失的4例(16.6%),肿瘤体积明显萎缩的12例(50.0%),肿瘤体积没有明显改变的6例(25%),肿瘤体积增大的2例(8.3%),肿瘤总控制率91.7%(22/24).19例颈神经孔神经鞘瘤患者伽玛刀治疗后肿瘤基本消失的3例(15.8%),肿瘤体积明显萎缩的9例(47.4%),肿瘤体积没有明显改变的6例(31.6%),肿瘤体积增大的1例(5.3%),肿瘤总控制率94.7%.本组患者肿瘤局部控制率为93%(41/44).临床症状改善总有效率为88.4%(38/43).结论 γ刀放射外科对非听神经性神经鞘瘤有良好的中长期控制作用,毒副作用较少.     

伽玛刀治疗颅底良性脑膜瘤长期疗效分析

目的总结评价伽玛刀(γ刀)治疗颅底良性脑膜瘤的长期疗效。方法217例患者平均年龄52.2±13.8岁(9～83岁),男性65例,女性152例;病史0.5～216个月,平均35.5个月,中位时间26个月;105例曾行手术治疗;肿瘤容积0.41～42.8cm3,平均6.8±6.1cm3;均行增强MRI定位扫描;边缘剂量10～20Gy,平均13.9±1.8Gy,中心剂量22.2～40Gy,平均27.7±4.6Gy;等剂量曲线40%～60%,平均49.53%;等中心数2～20个,平均10个。结果随访36～120(平均69.8±21.8)个月,肿瘤控制率为97.7%(212/217);临床表现:130例(59.9%)好转,78例(35.9%)稳定,9例(4.1%)恶化;9例曾出现一过性症状加重;2例(0.9%)出现放射性水肿;6例(2.8%)于γ刀后行显微外科手术切除。结论伽玛刀治疗颅底脑膜瘤可长期控制肿瘤生长,并发症较少,能保证患者良好的生存质量,即为术后残留或复发的患者提供了进一步治疗的方法,也为较小颅底脑膜瘤患者治疗的主要疗法。     

伽玛刀治疗海绵窦区的肿瘤

探讨各种海绵窦区肿瘤的诊断特点以及伽玛刀放射外科治疗的作用。文章回顾性地分析本中心1994年至2000年底Leksell伽玛刀治疗的168例累及海绵窦的各种肿瘤的临床资料,其中89例(53%)患者有开颅手术史,本组脑膜瘤88例,神经鞘瘤28例,垂体瘤22例,转移瘤14例,脊索瘤7例,海绵窦血管瘤4例,骨软骨瘤3例,巨细胞瘤1例和浆细胞瘤1例。全组肿瘤平均体积6.8mm3,给予肿瘤周边剂量7~18Gy,平均12.2Gy;中心剂量15~45Gy,平均26.7Gy;等中心曲线40%~80%,平均46%。有19例海绵窦病灶接受两次伽玛刀治疗。本组81.5%的病人随诊1~84个月,平均32.5个月。主要良性肿瘤…     

岩斜脑膜瘤的伽玛刀治疗

目的评估伽玛刀治疗岩斜区脑膜瘤的疗效。方法1995～2000年,我们对66例岩斜区脑膜瘤病人进行了伽玛刀治疗,肿瘤体积0.32～29.4cm3,平均(5.87±5.10)cm3。周边剂量为7～14.4Gy,平均(12.4±1.6)Gy;中心剂量16～65Gy,平均(27.9±5.9)Gy。结果60例随访25～94个月,平均(57.8±22.3)个月:肿瘤体积缩小23例(38.3%),不变35例(58.3%),增大2例(3.3%);神经系统症状好转37例(61.7%),稳定20例(33.3%),加重3例(5.0%)。无严重并发症发生。结论伽玛刀治疗能很好地控制肿瘤,副作用轻微,可作为神经外科较大肿瘤的辅助性治疗,也可作为较小肿瘤或不适合手术的病人的主要治疗。     

脑转移瘤的伽玛刀治疗

目的 评价伽玛刀治疗颅内脑转移瘤的疗效,分析能够预测预后生存率的因素.方法 407例脑转移瘤患者接受了伽玛刀治疗,随访344例,共756个病灶,肿瘤体积平均为(8.2±5.1)cm3,中心剂量和周边剂量分别(27.1±4.9)Gy和(15.4±2.0)Gy.对计数资料用X2检验,生存分析采用Kaplan-Meier曲线.结果 经过平均(17.7±9.8)个月的随访,影像学提示肿瘤消失140个、缩小331个、不变222个、增大63个.死亡病例114(33.1%)例,伽玛刀治疗后的平均生存期为(12.1±6.0)个月.年龄＜65岁、单发脑转移瘤、KPS≥70的患者有较好的生存率,且具有统计学意义(P＜0.01).结论 伽玛刀治疗脑转移瘤具有良好的控制率.年龄＜65岁、无颅外病变加重、KPS评分≥70、转移瘤灶少、原发灶控制,是具有良好生存期的预后因素.     

累及眶内肿瘤的伽玛刀治疗

目的 总结累及眶内肿瘤的伽玛刀治疗效果.方法 共治疗累及眶内的肿瘤患者35例,随访25例(脑膜瘤16例,脑膜血管外皮细胞瘤3例,神经鞘瘤2例,腺样囊性癌2例,转移癌1例,血管纤维瘤1例),采取1.5T PHILIPS或3.0T GE磁共振2 mm薄层扫描定位,Kula或GammaPlan剂量计划系统.肿瘤平均体积2.91 cm3(0.17～19.50 cm3),平均周边剂量12.4 Gy(8～15 Gy),中心剂量26.7 Gy(16～32 Gy).结果 本组随访期为1-62个月,平均30.4个月,23例控制满意,总体控制率为92%;6例(24%)症状减轻,13例(52%)症状无改变,5例(20%)出现了一过性的新发或原有症状加重;2例肿瘤增大,其中1例因突眼加重而行手术治疗.结论 对于累及眶内的较小病变、或经手术治疗后残留、复发等不宜手术治疗的病例,伽玛刀治疗可作为综合治疗的重要手段.     

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.