首发为Fisher综合征表现的肺癌转移致脑膜癌病一例

目的报告1例首发表现为Fisher综合征的脑膜癌病(MC),探讨其临床表现、影像及脑脊液(CSF)改变的特点。方法对1例首发症状表现Fisher综合征的MC进行病史采集和临床查体,分析其影像和CSF结果。结果患者以典型的Fisher综合征起病,后逐渐出现纳差、呕吐等颅高压表现,头颅MRI表现为脑干脑膜广泛强化,PET-CT提示肺癌并脑膜及骨转移。CSF发现肿瘤细胞。结论首发症状为Fisher综合征的肺癌转移致MC临床罕见,临床症状的多样性是MC容易误诊的主要原因。     

脑膜癌病21例临床分析

脑膜癌病 (meningealcarcinomatosis,MC)又称脑膜转移瘤 ,是指身体其他部位的恶性肿瘤转移到脑膜者 ,是颅内转移瘤的一种表现形式 ,该病病程进展快 ,平均生存期短 ,早期诊断困难 ,临床主要表现为头痛、呕吐 ,脑、脊神经麻痹 ,脑膜刺激征及精神障碍等。临床资料 :我院神经科发现原发病灶或 (和 )脑脊液(CSF)中发现肿瘤细胞确诊的MC患者 2 1例 ,其中男 9例 ,女 1 2例 ,年龄 42～ 79岁 ,平均年龄 (54± 1 1 )岁。有 1 9例发现原发灶 ,其中肺癌 1 5例 ,乳腺癌 2例、前列腺癌、肝癌、胃癌各 1例 ;1例在CSF中发现肿瘤细胞而未找到原发灶。急性…     

以痴呆为首发症状的脑膜癌病1例报告

脑膜癌病(meningeal carcinomatosis，MC)是肿瘤细胞广泛转移到脑膜和蛛网膜下腔的一种恶性疾病。临床表现为头痛、恶心、呕吐、脑膜刺激征、脑和脊神经麻痹及精神症状等。现报告以痴呆为首发症状的脑膜癌病1例。     

脑膜癌病的诊治进展

脑膜癌病（meningeal carcinomatosis，MC）又称脑膜转移瘤、柔脑膜转移或癌性脑膜炎，是恶性肿瘤细胞转移并弥漫性浸润软脑膜、蛛网膜下腔，临床表现为脑、脑神经和脊髓受损的症状，占所有肿瘤的3％～5％，位居中枢神经系统转移瘤的第3位。随着肿瘤患者生存期的延长以及影像技术的进步，其发病率逐年升高。虽然本病自首例报道至今已有140多年的历史，但是其研究进展却十分缓慢。随着分子生物学检测技术和靶向药物在临床中的广泛应用，本病的诊治有了一定的进步。     

卒中样表现脑转移瘤的影像学特征及预后研究

目的：分析卒中样表现脑转移瘤的影像学特点及预后的影响因素。方法选取2011‐03—2013‐05我院诊治的60例卒中样表现脑转移瘤患者,均进行C T或M RI检查,分析卒中样表现脑转移瘤患者的影像学特征,分析原发肿瘤部位、K PS全身功能评分、病理类型、脑转移瘤的数目、部位及不同治疗方式等对预后的影响。结果60例脑转移瘤患者中肺癌43例,乳腺癌5例,肝癌3例,肾癌4例,其他原发癌症5例;脑转移瘤的发生部位有多处,单纯脑膜转移患者较少;颅外器官转移者33例,无颅外器官转移者27例;原发灶发现前呈卒中样表现,多数患者具有神经功能障碍体征。影响脑转移瘤患者预后的因素主要为原发肿瘤部位、脑转移瘤数目、治疗方式、有无颅外器官转移等因素。结论卒中样表现脑转移瘤采用CT检查能够有效反映病理特征,对于预后判断有一定的参考价值,为临床指导脑转移瘤预后恢复提供了参考依据。     

8例脑膜癌病临床与脑脊液细胞学分析

脑膜癌病（Meningeal Carcinomatosis，MC）亦称癌性脑膜炎，系中枢神经系统转移瘤的一种少见类型，是恶性肿瘤通过血行转移或脑脊液种植播散而累及脑膜，脑、脊髓内并无明显肿块的一种非独立性的严重疾病，此病确诊主要依赖脑脊液细胞学。本文结合文献资料，对2年来经脑脊液细胞学诊断的8例MC临床资料进行回顾分析。     

脑膜癌病1例

脑膜癌病（meningeal carcinomatasis,MC）又称癌性脑膜炎,是肿瘤细胞在脑、脊髓蛛网膜下腔和软脑膜内弥漫性转移并随血管周围间隙侵入脑实质而引起的一系列临床综合征,由于MC原发病灶隐匿,转移形式特殊,临床表现缺乏特异性,一般常规影像学检查无异常发现,早期诊断较困难.现将我科收治的1例脑膜癌患者进行报告如下.     

63例脑膜转移瘤预后因素分析

目的 探讨脑膜转移瘤(CM)的预后因素.方法 对天津医科大学附属肿瘤医院自1998年至2008年确诊的63例CM患者的临床资料进行回顾性分析,主要分析因素有性别、年龄、原发灶类别、KPS评分、确诊原发灶与发现脑膜转移瘤间隔时间、治疗方式、放疗剂量、原发灶控制情况等,Kaplan-Meier法计算生存期并绘制生存曲线,log-rank法进行检测验证,Cox多因素回归模型进行预后分析.结果 截止到随访结束,所有患者均已死亡,总生存期为2～732d,1年生存率为7.9%(5/63),中位生存期为67 d.Cox模型多因素分析显示KPS评分、原发灶控制情况、确诊原发灶与发现脑膜转移瘤间隔时间为独立预后因素.结论 CM主要预后因素为KPS评分、原发灶控制情况、确诊原发灶与发现脑膜转移瘤间隔时间.CM最佳治疗模式有待进一步研究,针对患者具体情况的个体化治疗值得在临床推广.     

基于MRV误诊为静脉窦血栓形成的脑膜癌病1例报告

正脑膜转移瘤(MC)是不同于脑实质转移瘤或硬膜外转移伴脊髓受压的一种CNS转移瘤,常缺乏定位体征,且转移累及脑膜和CSF时MRI平扫显示其与周围正常组织并无差异,故临床上容易误诊误治。我科近日收治乳腺癌术后脑膜转移、骨转移1例,该病例先前基于MRV而误诊为静脉窦血栓     

脑膜癌瘤病（附5例临床分析）

脑膜癌病系癌肿向颅内转移的一种特殊类型,癌细胞弥散浸润软脑膜或脊膜,而颅内无占位性病灶。临床表现以脑、颅神经、脊神经损害为主等症状。多在病程中能发现原发灶,但较隐匿,部分病例也可先于原发灶表现于临床。本文5例经脑脊液细胞学检查证实为脑膜癌病。现分析报导如下: 临床资料 (一).一般资料:5例均为女性,年龄最小32岁,最大69岁,平均45.4岁,30～40岁3例乳腺癌1例,肺癌1例,甲状腺癌1例,粘液癌1例,原发灶不明1例。5例均经脑脊液细胞学检查发现癌细胞。均经头部CT扫描排除颅内占位性转移。 (二).临床表现:本组从发病至就诊时间最短7天,最长3个月,平均55天。首发症     

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.