氢质子磁共振波谱在儿童创伤性颅脑损伤的应用

目的 探讨氢质子磁共振波谱( 1H-MRS)分析对儿童创伤性颅脑损伤(TBI)受伤程度及预后的临床价值.方法 对20例儿童TBI病人(TBI组)和10例正常儿童志愿者(正常对照组)进行1H-MRS检查,观察两组病侧与对侧N-乙酰天门冬氨酸(NAA)、胆碱(Cho)、肌酸(Cr)、乳酸(Lac)及NAA/Cr、NAA/Cho、Cho/Cr比值的变化,分析这些指标与GCS及GOS评分的相关性.结果 与正常对照组比较,TBI组NAA/Cho、NAA/Cr比值明显下降(P＜0.05),而Cho/Cr比值明显升高(P＜0.05);TBI组出现Lac峰1例,最终死亡.而NAA/Cr、NAA/Cho比值变化与GCS评分呈负相关(r=-0.59,P＜0.05),与GOS 呈正相关(r=0.63,P＜0.05);TBI组Cho/Cr比值与GCS评分呈正相关(r=0.57,P＜0.05),与GOS评分呈负相关(r=-0.69,P＜0.05).结论 1H-MRS对判断颅脑损伤的受伤程度及预后有重要参考价值.     

颅脑损伤后神经递质系统变化与认知障碍的研究进展

近年来,颅脑损伤(traumatic brain injury,TBI)的发生率、致残率逐渐增高,随着对脑外伤急性期治疗F段的不断提高,已能大大降低早期的死亡率.然而,它仍是慢性期致残的主要原因,其中认知功能障碍是最持久和最严重的症状之一[1].虽然大部分患者中这些功能在1年后恢复正常,但仍有10％～15％的轻型脑损伤患者存在功能障碍,在中、重型TBI患者中比例更高[2].TBI后认知障碍的确切机制至今仍不十分清楚,研究发现大脑内学习和记忆等认知活动与多种神经递质相关,包括乙酰胆碱(acetylcholine,Ach),去甲肾上腺素,多巴胺(DA),5-羟色胺(5-HT),γ-氨基丁酸,谷氨酸,神经营养因 子等[3].本文就TBI后主要神经递质系统的变化及其与认知障碍的研究进展进行简要综述.     

帕金森病异质性的质子磁共振波谱研究

目的利用质子磁共振波谱(1 H-MRS)技术研究不同运动亚型原发性帕金森病(IPD)患者纹状体、额叶皮质运动区的变化,并比较其认知障碍的发生率,研究帕金森病认知障碍(PD-CIND)患者海马区的变化,探讨1 H-MRS在IPD诊断及分型诊断的价值。方法对70例IPD患者行帕金森病统一评分量表(UPDRS)运动障碍评分,并进行临床分型,依据主要运动症状分为震颤为主型IPD 38例、姿势异常、步态障碍(PIGD)型IPD 32例,同时对各运动亚型行蒙特利尔认知量表评分(MOCA),选出MOCA26分的PD-CIND患者共27例,无认知障碍IPD(MOCA≥26分)患者43例,健康对照组(HC)30例,对各组双侧纹状体,额叶皮质运动区、海马区行1 H-MRS检测,计算N-乙酰天门冬氨酸/肌酸(NAA/CR)和胆碱复合物/肌酸(CHO/CR)的比值。结果震颤为主型IPD伴发认知障碍10例。PIGD型IPD伴发认知障碍17例,2组比较有显著性差异(P0.05),IPD组纹状体、额叶皮质运动区NAA/CR比值较HC组明显下降(P0.05),震颤为主型IPD双侧纹状体、额叶皮质运动区NAA/CR比值高于PIGD型IPD(P0.05),PD-CIND组海马区NAA/CR比值低于IPD组及HC组(P0.05)。而各组CHO/CR比值差异均无统计学意义(P0.05)。结论 IPD患者双侧纹状体、额叶皮质运动区NAA/CR比值降低,尤以PIGD型IPD下降明显,同时震颤为主型PD认知障碍伴发率低于PIGD型,而IPD患者海马区NAA/CR比值降低,尤以PD-CIND患者下降明显,1 H-MRS有助于IPD的诊断及分型诊断。     

创伤性脑损伤后认知障碍研究现状

创伤性脑损伤(traumatic brain injury,TBI)具有较高的发生率,尤其是在当代社会工业和经济高度发达的社会中.TBI后遗症多,残、死率高,不仅给患者本人及其家庭带来了巨大痛苦,也对社会造成了沉重的负担.TBI的严重后果包括:①运动功能缺陷;②知觉障碍;③认知缺陷;④语言障碍;⑤人格改变等.认知障碍为TBI最常见、最持久的后遗症状之一.本文就TBI后认知障碍的研究现状进行简要概述.     

颞叶癫痫患者海马硬化与认知障碍的相关性分析

目的探讨颞叶癫痫(temporal lobe epilepsy,TLE)患者海马硬化(hippocampal sclerosis,HS)与认知障碍的关系。方法采集TLE患者起病年龄、病程、有无高热惊厥史、有无全面强直阵挛发作(generalized tonic clonic seizure,GTCS)等相关病史,行海马氢离子磁共振波谱成像(~1H-Magnetic resonance spectroscopy,1H-MRS)分析海马组织细胞N-乙酰天门冬氨酸(NAA)、胆碱(Cho)及肌酸(Cr)浓度,计算NAA/(Cho+Cr)值,并运用《中国修订版韦氏成人智力量表》和《中国修订版韦氏成人记忆量表》对认知功能进行评测,分析HS与认知障碍的关系。结果起病年龄越小、病程越长,有高热惊厥史、有GTCS发作等因素的患者海马NAA/(Cho+Cr)值更低,认知障碍更严重(P0.05);伴HS的TLE患者比不伴HS的TLE患者认知障碍严重,且两者较正常人严重(P0.05);HS患者海马NAA/(Cho+Cr)值下降程度与认知障碍程度有明显相关性(P0.05)。结论 TLE患者起病年龄、病程、高热惊厥史、GTCS发作等病史与认知障碍相关;对TLE患者行海马~1H-MRS检查有助于早期评估及发现认知障碍,为临床合理选择抗癫痫药物、添加改善认知障碍药物、改善患者生活质量提供依据。     

创伤性脑损伤后认知障碍发生机制的研究进展

创伤性脑损伤(traumatic brain injury,TBI)也称为脑外伤,其发生率高、死残率高、后遗症多,给患者及家庭造成极大的痛苦和经济负担也给社会带来沉重的负担.TBI的严重后果包括:运动功能缺陷、知觉障碍、认知缺陷、语言障碍、外伤性癫痫、人格改变等,其中认知障碍为最持久和最严重的症状之一,通常表现在注意力和记忆力两方面.研究表明空间记忆缺失发生于各种程度的TBI之后,而有关TBI之后认知障碍的确切机制至今仍不十分清楚.     

创伤性脑损伤后认知障碍发生机制的研究进展

创伤性脑损伤(traumatic brain injury,TBI)也称为脑外伤,其发生率高、死残率高、后遗症多,给患者及家庭造成极大的痛苦和经济负担也给社会带来沉重的负担.TBI的严重后果包括:运动功能缺陷、知觉障碍、认知缺陷、语言障碍、外伤性癫痫、人格改变等,其中认知障碍为最持久和最严重的症状之一,通常表现在注意力和记忆力两方面.研究表明空间记忆缺失发生于各种程度的TBI之后,而有关TBI之后认知障碍的确切机制至今仍不十分清楚.     

创伤性脑损伤后认知障碍发生机制的研究进展

创伤性脑损伤(traumatic brain injury,TBI)也称为脑外伤,其发生率高、死残率高、后遗症多,给患者及家庭造成极大的痛苦和经济负担也给社会带来沉重的负担.TBI的严重后果包括:运动功能缺陷、知觉障碍、认知缺陷、语言障碍、外伤性癫痫、人格改变等,其中认知障碍为最持久和最严重的症状之一,通常表现在注意力和记忆力两方面.研究表明空间记忆缺失发生于各种程度的TBI之后,而有关TBI之后认知障碍的确切机制至今仍不十分清楚.     

创伤性脑损伤后认知障碍发生机制的研究进展

创伤性脑损伤(traumatic brain injury,TBI)也称为脑外伤,其发生率高、死残率高、后遗症多,给患者及家庭造成极大的痛苦和经济负担也给社会带来沉重的负担.TBI的严重后果包括:运动功能缺陷、知觉障碍、认知缺陷、语言障碍、外伤性癫痫、人格改变等,其中认知障碍为最持久和最严重的症状之一,通常表现在注意力和记忆力两方面.研究表明空间记忆缺失发生于各种程度的TBI之后,而有关TBI之后认知障碍的确切机制至今仍不十分清楚.     

创伤性脑损伤后认知障碍发生机制的研究进展

创伤性脑损伤(traumatic brain injury,TBI)也称为脑外伤,其发生率高、死残率高、后遗症多,给患者及家庭造成极大的痛苦和经济负担也给社会带来沉重的负担.TBI的严重后果包括:运动功能缺陷、知觉障碍、认知缺陷、语言障碍、外伤性癫痫、人格改变等,其中认知障碍为最持久和最严重的症状之一,通常表现在注意力和记忆力两方面.研究表明空间记忆缺失发生于各种程度的TBI之后,而有关TBI之后认知障碍的确切机制至今仍不十分清楚.     

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.