颅咽管瘤术后钠代谢紊乱分析

目的 分析颅咽管瘤全切除术后钠代谢紊乱的诊断及处理。方法 对51例巨大颅咽管瘤全切除患者进行回顾性分 析,根据血、尿钠以及中心静脉压等确定钠代谢紊乱类型,并进行相应处理。结果 发生低钠血症29例(56.7％),高钠血症13例 (25.5％)。本组2例死亡,高钠及低钠血症交替9例(17.6％)。高钠及低钠血症平均开始时间分别为术后2.3 d和4.8 d。结论 钠 代谢紊乱是颅咽管瘤全切除术后常见表现之一,必须根据具体的紊乱类型进行治疗。     

颅咽管瘤切除术后常见并发症的处理

目的 探讨颅咽管瘤切除术后常见并发症的特点和处理。方法 对我科80例颅咽管瘤切除患者的临床资料进行回顾性分析。结果 术后出现尿崩72例，出院时39例尿量恢复正常，仍有尿崩者33例；钠代谢紊乱58例，其中低钠血症31例，高钠血症14例，高钠、低钠交替13例，出院时血钠正常者51例，仍有钠代谢紊乱者7例；高热34例，出院时体温均正常；意识障碍20例，1例因长期昏迷死于循环功能衰竭，出院时11例意识清楚，8例仍有意识障碍；癫痫5例。1例死于癫痫持续状态，余4例得到良好控制。结论 处理尿崩时要合理使用抗利尿制剂。引起低钠的原因有脑性盐耗综合征和抗利尿激素异常分泌综合征，治疗前者应补液、补盐。后者应适当限水、利尿。高钠血症要限钠、补液并给予抗利尿制剂。发生高热应及时降温。出现意识障碍，除做CT检查确定有无颅内血肿和脑积水外。还应从电解质和激素用药方面查找原因。癫痫是颅咽管瘤术后极危险的并发症，要及时控制。避免出现癫痫持续状态。     

颅咽管瘤切除术后低钠血症的诊断和治疗

目的探讨颅咽管瘤切除术后低钠血症的病理生理、诊断和治疗。方法对我科收治的44例颅咽管瘤切除术后发生低钠血症患者的临床资料进行回顾性分析,根据临床症状、实验室检查、中心静脉压确定低钠的程度及类型并进行相应处理。结果除2例病人自动出院外,其余病人的低钠血症得到良好纠正。结论颅咽管瘤术后低钠血症的发生率很高,引起低钠的原因有脑性盐耗综合征和抗利尿激素异常分泌综合征,治疗原则各不同,前者要补液、补盐,后者要适当限水、利尿。     

颅咽管瘤全切除术后低钠血症的诊断及处理

目的：探讨颅咽管瘤全切除患术后发生低钠血症的诊断及处理方法。方法: 回顾性分析我科近4年颅咽管瘤全切除术后并发低钠血症的36例患。根据实验室检查、 临床症状及中心静脉压确定低钠血症的类型并给予对症处理。结果：1例死于继发性脑梗塞，1例自动出院，34例患低钠血症状恢复。结论：中枢性低钠血 症包括脑性盐耗综合征（CSWS）和抗利尿激素不适当分泌综合征（SIADH）。前应予以充分补钠、补水,可通过肠内及静脉两种方式进行补充；后却需要限水治疗。     

脑肿瘤切除术后脑性耗盐综合征的临床研究

目的　探讨脑肿瘤切除术后脑性耗盐综合征 (CSWS)的病因、类型、诊断及处理方案。方法　分析 2 3 4例脑肿瘤术后出现 2 1例脑性耗盐综合征的病例资料及诊疗情况 ,患者多在术后第 4～ 9天出现血钠下降 ,血钠均低于 13 0mmol/L ,2 4h尿钠排泄均超过 10 0mmol,CVP <6cmH2 O。结果　 18例一过性低钠血症 ,经充分补钠、补液治疗 4～ 9d后恢复正常 ;1例颅咽管瘤患者术后第 10天死亡 ;2例持续性低钠血症患者病情明显恶化 ,但补钠效果不佳。结论　鞍区肿瘤术后CSWS发生率较高 ,常伴有尿崩症 ;颅咽管瘤术后CSWS发生率较垂体瘤术后高 ,血钠降幅更显著。CSWS存在一过性和持续性两种类型。     

儿童颅咽管瘤术后血钠水平的波动及其与癫痫发作的关系

目的探讨儿童颅咽管瘤患者术后7 d内血钠水平的波动及其与癫痫发作的关系。方法回顾性分析74例颅咽管瘤手术患儿的临床资料。其中术后发生癫痫者6例(8.1%)。检测患儿术后当日、术后1~7 d及发生癫痫时的血钠浓度,血钠值正常范围为135~145 mmol/L。依据各时间点的血钠值将患儿分为4组,均在正常范围者为血钠正常组,持续性低钠血症者为低钠血症组,持续性高钠血症者为高钠血症组,既有高钠血症也存在低钠血症者为交替异常组。分析患儿术后7 d血钠波动状况及各组患儿的癫痫发生率。结果本组74例患儿术后1~3 d的平均血钠值均在正常范围;术后4~6 d的平均血钠值均低于正常,第4 d为低钠血症的高发时间点;术后第7 d平均血钠值恢复至正常水平。74例患儿中,交替异常组26例(35.1%),其中发生癫痫者5例(19.2%);低钠血症组9例(12.2%),发生癫痫者1例(11.1%);血钠正常组22例(29.7%),高钠血症组17例(23.0%),均无发生癫痫者。结论术后第4 d为颅咽管瘤患儿低钠血症的高发时间点;颅咽管瘤患儿术后血钠水平降低,更有可能导致癫痫发作。     

颅咽管瘤全切术后抗利尿激素分泌异常综合征的治疗

目的 探讨颅咽管瘤全切术后抗利尿激素分泌异常综合征(SIADH)的临床特点及治疗方法。方法 120例颅咽管瘤切除术病人，112例肿瘤全切除，手术当日及术后每日定时检测血钠及观察尿量变化。17例病人术前、术后当日、术后3d、7d、14d检测血清抗利尿激素(ADH)水平，并进行比较观察。结果 ①72例(60％)术后出现以低血钠为主要特征的抗利尿激素分泌异常综合征。其中37例(51.4％)单纯性低血钠，29例(40.3％)尿崩症伴高血钠后转为低血钠，6例(8.3％)低血钠后转为尿崩症伴高血钠。②17例病人术前、术后当日、术后3d、7d、14d血清ADH放射免疫学测定，示术后SIADH病人血清ADH水平与术前相比有所增高，但是经统计学分析无显性差别。结论 颅咽管瘤全切术后SIADH为常见术后合并症，可能是由于颅咽管瘤术后下丘脑ADH的释放不能随着体内晶体渗透压变化而改变所致。术前和术后2周内血清ADH水平变化没有显性差异。     

儿童颅咽管瘤术后水电解质紊乱的管理方案

目的 探讨儿童颅咽管瘤术后水电解质紊乱的管理方案。方法 回顾性分析2016年12月到2019年5月手术治疗的56例儿童颅咽管瘤的临床资料。术后高钠血症使用生理盐水补充每日钠需要量+5%葡萄糖溶液降血钠,术后出现重度低钠血症使用3%盐水微量泵持续补钠。结果 术后出现尿崩症40例（71.4%）,电解质紊乱30例（53.6%）。高钠血症患儿治疗第一天血钠波动幅度平均为（7.8±2.0） mmol/L,第二天平均为（5.9±2.2） mmol/L,控制时间平均（76.5±11.7）h。重度低钠血症患儿治疗第一天波动幅度平均为（7.7±2.0） mmol/L,第二天平均为（7.5±3.1） mmol/L,控制时间平均（89.8±14.2）h。治疗过程中,未出现意识障碍、癫痫、脱髓鞘等并发症。出院时,40例尿崩症患儿的尿量得到控制,30例电解质紊乱患儿连续3次血清Na+正常。结论 儿童颅咽管瘤术后电解质紊乱发生率高,稳定血清钠波动幅度,有助于改善病人预后。     

50例多发性额叶挫裂伤术后水钠代谢紊乱的分析

目的分析额叶挫裂伤术后水钠代谢紊乱的病理生理、诊断及处理。方法额叶挫裂伤50例,术后每4h取标本测定血钠、尿钠、渗透压以及中心静脉压等连续7d,测定水钠值,分析水钠代谢紊乱类型,进行治疗处理。结果本组发生低钠血症28例(56%),高血钠10例(20%),高钠及低钠交替出现12例(24%),高钠及低钠血症平均发生时间为术后24～36h和72～86h,ICU综合治疗,钠代谢紊乱均获得纠正,平均住院28d。2例死于严重下丘脑反应。结论水钠代谢紊乱是额叶多发性挫裂伤术后常见表现。高血钠与尿崩有密切关系,低钠血症则为脑性耗盐综合征和抗利尿激素分泌不适当相关。二者的临床处理方法:高钠血症应在颅内压监测指导下补足液体和高钠盐液,而低钠血症则应在补盐的基础上要适当限水和利尿。     

QST分型对儿童颅咽管瘤术后血钠水平异常的影响

目的探讨不同QST分型颅咽管瘤患儿术后血钠水平异常的发生特点。方法回顾分析2016年1月至2017年6月经外科手术治疗的48例原发性颅咽管瘤患儿的临床、影像学及手术资料,分析不同QST分型对患儿术后血钠水平的影响及差异性。结果(56.25%),中至重度12例次占25%;高钠血症32例次(66.67%),中至重度16例次占33.33%。不同分型组患儿低钠血症(χ~2=11.420,P=0.003)和高钠血症(χ~2=15.702,P=0.000)发生率差异具有统计学意义,其中T型颅咽管瘤患儿术后中至重度低钠血症(Z=-3.324,P=0.001)和中至重度高钠血症(Z=-3.874,P=0.000)发生率高于Q型;单因素Logistic回归分析显示,QST分型是术后发生中至重度血钠水平异常的重要影响因素,T型为其危险因素(OR=315.422,95%CI:16.804～5920.786;P=0.000)。结论颅咽管瘤患儿术后应进行血钠水平长期监测,QST分型有助于预测血钠水平异常的发生及其严重程度,T型颅咽管瘤患儿可能为术后血钠水平异常的易感者。     

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.     

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 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.     

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.     

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.     

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.     

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.     

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.