颅脑外伤后低钠血症与血清脑钠素抗利尿激素醛固酮的关系

目的探讨颅脑外伤后低钠血症与脑钠素、抗利尿激素和醛固酮的关系及其发病机制。方法测定42例颅脑损伤患者伤后第1、5、7、10天不同时间点血钠、尿钠、脑钠素、抗利尿激素和醛固酮的浓度。结果 15例患者(44.1%)出现低钠血症,较无低钠血症者血醛固酮浓度显著降低,抗利尿激素浓度显著升高。结论低钠血症的发生与醛固酮分泌减少、抗利尿激素分泌增加有关。     

重型颅脑外伤后低钠血症的相关因素分析及处理

目的 :探讨重型颅脑外伤后并发低钠血症的因素、发生机制、病理生理、诊断和治疗。方法 :①监测血生化、血气分析、尿比重、尿电解质等。②记录 2 4h出入量。③限水治疗结果 :CSWS 2例 ,SIADH 7例。结论 :重型颅脑外伤后低钠血症是由于脱水、利尿导致排钠大于摄入所致 ,而难治性低钠血症应考虑有SIADH和CSWS存在的可能 ,CSWS与ANP有关     

重型颅脑外伤后低钠血症的相关因素分析及处理

目的：探讨重型颅脑外伤后并发低钠血症的因素、发生机制、病理生理、诊断和治疗。方法：①监测血生化、血气分析、尿比重、尿电解质等。②记录24h出入量。③限水治疗结果：CSWS2例,SIADH7例。结论：重型颅脑外伤后低钠血症是由于脱水、利尿导致排钠大于摄入所致,而难治性低钠血症应考虑有SIADH和CSWS存在的可能,CSWS与ANP有关。     

重型脑外伤患者血浆抵抗素水平动态变化与预后的关系

目的:研究血浆抵抗素水平与重型脑外伤预后的相关性。方法:取80例重型脑外伤患者在入院时及入院后第1、2、3、5、7天静脉血,另取80例体检健康者静脉血做对照。用ELISA法测定血浆抵抗素浓度,分析血浆抵抗素水平与格拉斯哥(GCS)评分及死亡的相关性,以及抵抗素水平对重型脑外伤患者1个月内死亡的预测特异度和敏感度。结果:脑外伤后第1、2、3、5、7天血浆抵抗素水平明显增高。入院时血浆抵抗素水平增高是脑外伤1个月内死亡的危险因素(P=0.042),与入院时GCS评分呈显著负相关(P<0.001),对脑外伤后患者1个月内死亡有显著预测价值(P<0.001)。结论:脑外伤后血浆抵抗素水平显著增高,可作为重型脑外伤患者预后判断的重要指标。     

重型颅脑损伤后低钠血症临床与预后分析

目的探讨重型颅脑损伤后低钠血症的发病因素,处理方法及其对预后的影响。方法回顾性分析124例重型颅脑损伤患者的临床资料。结果低钠血症可进一步加重脑水肿,且并发低钠血症、继发性脑梗死、脑积水的发生率均显著高于血钠正常者(P<0.05)。结论重型颅脑损伤后低钠血症发生率很高是预后差的危险因素,其主要原因为脑性盐耗综合征和抗利尿激素分泌失调综合征,应针对病因治疗。     

急性重型颅脑损伤后脑性盐耗综合征49例临床分析

目的探讨急性重型颅脑损伤后脑性盐耗综合征（CSWS）的临床特点、诊断和治疗方法。方法回顾性分析49例急性重型颅脑损伤后CSWS患者的临床资料。结果所有患者血清钠均低于130mmol／L,24h尿钠均大于80mmol,L,血浆渗透压小于270mos／L;36例患者血脑钠肽或脑钠肽前体增高。治疗6～22d后,46例患者血钠恢复正常,1例由于放弃治疗而死于低钠血症,2例死于肺部感染。结论低血钠、高尿钠、低血容量、对补充血容量和补钠治疗有效是CSWS的临床特点及诊断依据;及时监测血钠水平并予补钠、补液治疗安全有效。     

重型颅脑外伤后血管痉挛与脑脊液NO及内皮素水平的关系

目的探析重型颅脑外伤后脑血管痉挛(CVS)和脑脊液一氧化氮(NO)及内皮素(ET-1)水平的相关性。方法入选我院2012-02—2014-02收治的重型颅脑外伤后CVS患者124例作为观察对象,根据CVS严重程度分为重度组40例,中度组42例,轻度组42例,入选同期重型颅脑外伤后未发生CVS的40患者作为对照组,检测患者入院后1d、3d、5d及7d时双侧大脑中动脉(MCA)和颈内动脉颅外段(ICA)脑血流速度及脑脊液NO、ET-1水平。结果 CVS各组NO浓度均显著低于对照组,且CVS重度组NO浓度显著低于中度组,中度组显著低于轻度组;ET-1呈相反变化。结论颅脑外伤后CVS的发生可能与脑脊液中NO抑制,ET-1升高,破坏血管舒张收缩平衡相关。     

重型颅脑损伤患者血浆8-表氧前列腺素F2α水平及抗氧化剂疗效评价

目的探讨8-表氧前列腺素F2α(8-iso-PGF2α)在重型颅脑损伤患者血浆中的水平和在抗氧化剂疗效评估中的价值。方法对自2003年1月至2004年12月收住的98例重型颅脑损伤患者以2004年4月为界分为前期68例,后期30例。前期病例根据随机原则分成:常规治疗组和加用抗氧化剂VitC VitE治疗组,各34例;后期病例给予新型抗氧化剂依达拉奉治疗。同时设健康体检者对照组40例。在受伤第1、2、3、7、14、30天,分别对存活患者清晨空腹采取肘静脉血3mL,对照组亦同。采用ELISA法测定血浆8-iso-PGF2α含量。以三个月为限,根据GOS标准分成死亡、恢复不良(包括植物生存、重残与中残)和恢复良好。结果用抗氧化剂治疗组受伤第7天、第14天血浆8-iso-PGF2α检测值比常规治疗组明显下降(P<0.05)。而常规治疗组两周内5次血浆8-iso-PGF2α的检测值均高于对照组(P<0.01)。伤后3月时,VitC VitE治疗组死亡率41.18%,常规治疗组死亡率64.71%,依达拉奉治疗组死亡率33.33%。结论抗氧化剂能够明显降低重型颅脑损伤患者血浆8-iso-PGF2α的水平,依达拉奉能显著降低重度颅脑损伤患者死亡率。血浆8-iso-PGF2α的动态变化能够作为重型颅脑损伤患者抗氧化剂疗效评估的一项有效的生化指标。     

颅脑创伤后并发低钠血症118例诊疗分析

目的探讨颅脑创伤后并发低钠血症的临床特点及中枢性低钠血症的诊治经验。方法回顾性分析2005年1月至2011年1月我院神经外科收治的118例并发低钠血症的颅脑创伤患者的临床资料,通过临床表现及实验室检查明确诊断,探索有效的治疗方案。结果本组治愈103例(87.3%),死亡15例(12.7%),其中放弃治疗2例,死于各种并发症13例,无低钠血症死亡病例。轻中型、重型及特重型颅脑损伤患者的中重度低钠血症发生率分别为37.0%、54.3%和76.2%(χ2=7.296,p=0.026);三种类型颅脑损伤患者的低钠血症持续时间超过8天的发生率分别为48.1%、50.0%和85.7%(χ2=9.220,p=0.010)。诊断为脑性盐耗综合征(CSWS)22例(18.6%),抗利尿激素不适当分泌综合征(SIADH)7例(5.9%),营养性低钠血症89例(75.5%)。CSWS组和SIADH组中血钠浓度与营养性低钠血症组相比无显著性差异(t=-0.896,p=0.609);血浆ADH及血浆渗透压与营养性低钠血症组相比存在显著性差异(t≥130.31,p0.05)。结论颅脑损伤越重,发生中重度低钠血症可能性越大,低钠血症持续时间越长。CSWS组血浆ADH显著低于营养性低钠血症组,SIADH组血浆ADH显著高于营养性低钠血症组,CSWS组和SIADH组血浆渗透压均低于营养性低钠血症组。CSWS和SIADH是导致颅脑创伤后低钠血症的主要原因,两者在发病机制、临床诊断及治疗方面都存在明显区别。早期诊断,及时明确类型,针对性积极治疗,可有效降低患者致残率和致死率,改善预后。     

颅脑外伤患者免疫水平及感染风险的分析研究

目的 探讨不同程度颅脑外伤患者的免疫功能、感染风险及对预后的影响。方法 南京大学医学院附属南京鼓楼医院重症医学科2016年9月—2019年9月收治的急性颅脑外伤患者86例;按格拉斯哥昏迷量表(Glasgow coma scale,GCS)评分标准分为轻中型组(24例)和重型组(62例)。收集两组患者入院时一般资料、炎症指标及免疫指标;并统计入院1～3 d、4～7 d、7～14 d内的新增感染患者例数及入院14 d内的死亡例数。以入院14 d内出现死亡为预后指标,分析影响颅脑外伤患者入院14 d内预后的相关因素。结果与重型组相比,轻中型组患者的血白细胞(WBC)计数、C反应蛋白(C-reactive protein,CRP)、血降钙素原(procalcitonin,PCT)水平均显著降低,血淋巴细胞(CD4+、CD8+)、人类白细胞抗原-DR(human leukocyte antigen-DR,HLA-DR)水平均显著升高。经多因素Logistics回归分析显示,WBC、PCT、入院后第1～3 d内发生感染是影响预后的独立危险因素,HLA-DR是影响预后的独立保护因素。结论 重型颅脑外伤患者比轻中型患者的免疫功能更低下、感染出现时间更早、感染程度更重,且易合并多部位感染。早期血WBC、PCT水平、入院后第1～3 d内发生感染是影响患者生存的独立危险因素;而HLA-DR是影响生存的独立保护因素。入院时应评估患者的感染情况及免疫功能,并动态监测;尽早控制感染、提高免疫水平,以改善患者的预后。     

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.     

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.     

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.     

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.     

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.     

Effects of NMD A- and AMPA-Receptor Antagonists on Different Forms of Epileptiform Activity in Rat Temporal Cortex Slices

Summary: Lowering extracellular magnesium induces different patterns of epileptiform activity in rat hippocampus and entorhinal cortex. Short recurrent epileptiform discharges in the hippocampus are stable over time, whereas seizurelike events (SLEs) in the entorhinal cortex, the subiculum, and the neighboring neocortex develop into late recurrent discharges which are not blocked by clinically employed antiepileptic drugs. We tested the sensitivity of the different epileptiform discharge patterns to. /V-methyl-D-aspartate (NMDA)- and non-NMDA-receptor antagonists. As NMDA-receptor antagonist we used dextrorphan, ket-amine, and 2-aminophosphonovalerate (2APV); as α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA)-receptor antagonist we employed the quinoxaline derivative glutamate 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). The findings show that the different patterns of epileptiform activity, including the late recurrent discharges, are sensitive to all NMDA-receptor antagonists. However, when dextrorphan was employed to suppress seizure-like events, later recurrent discharges did not develop during the remaining time course of the experiment. CNQX reversibly suppressed recurrent discharges in the hippocampus and SLEs in the entorhinal cortex. However, late recurrent discharges become insensitive to CNQX, even at a high concentration of 60 μM m. This finding suggests a prominent role for NMDA receptors in the generation of late recurrent discharges.     

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.