高同型半胱氨酸血症与卒中的关系

目的 探讨高同型半胱氨酸（Homocysteine,Hcy）血症与卒中的关系。方法 选择卒中患者102例（66例脑梗死和36例脑出血）为卒中组,与病例组年龄、性别、种族等相匹配的未患过卒中来院进行健康体检者102例为对照组。采用高效液相色谱荧光检测法测定两组的血清Hcy水平。同时检测叶酸、维生素B12、血糖、血脂等。结果 卒中组血清Hcy水平显著高于对照组（20±9μmol/L vs 9±6μmol/L,P<0.01）;脑梗死和脑出血患者的血清Hcy水平无统计学差异（P>0.05）;血清叶酸及维生素B12水平与血清Hcy均呈负相关;Logistic回归分析显示,高Hcy血症卒中的独立危险因素（OR 4.875,95%CI 1.902～8.552,P<0.05）。结论 高Hcy血症是卒中的独立危险因素;叶酸和VitB12的缺乏可能是导致高Hcy血症的原因之一。     

叶酸和维生素B6、B12联合治疗青年脑卒中合并高同型半胱氨酸血症的疗效观察

目的 观察叶酸和维生素B6、B12联合治疗青年脑卒中合并高同型半胱氨酸(Hcy)血症的疗效.方法 将150例青年脑卒中合并高Hcy血症患者随机分为低剂量叶酸和维生素B6、B12治疗组(低剂量组)、高剂量叶酸和维生素B6、B12治疗组(高剂量组)、对照组,每组50例.用药剂量:低剂量组给予叶酸2.5mg/d、维生素B6 10 mg/d、维生素B12 0.5 mg/d,高剂量组给予叶酸5 mg/d、维生素B6 30 ms/d、维生素B12 1.5mg/d,连续给药4周,对照组不予叶酸和维生素B6、B12治疗.治疗前后检测血浆Hcy浓度,治疗后血浆Hcy浓度＜15 μmol/L为有效;并观察不良反应.结果 治疗4周后低剂量组、高剂量组临床有效率分别是70.4%、71.6%,与对照组(4.6%)相比差异有统计学意义(均P＜0.01);治疗后低剂量组、高剂量组血浆Hcy浓度比治疗前明显降低(下降33.9%和36.1%)(均P＜0.01);对照组治疗后的血浆Hcy浓度无明显下降.3组治疗过程中均未出现不良反应.结论 叶酸和维生素B6、B12联合治疗青年脑卒中合并的高Hcy血症有明显效果,而且高、低两种剂量均有效;无不良反应.     

血浆同型半胱氨酸与颅内动脉瘤的关系

目的 探讨血浆同型半胱氨酸(Hcy)、血清叶酸、维生素B12水平与颅内动脉瘤的关系.方法 采用化学发光法检测80例颅内动脉瘤患者和60例对照者血浆Hcy、血清叶酸、维生素B12水平,相关危险因索用logistic回归分析.结果 颅内动脉瘤组平均血浆Hcy水平明显高于对照组(P=0.005),两组中血浆Hcy升高分别有38例(48%)和9例(15%)(X2=16.239,P＜0.001);颅内动脉瘤组平均血清叶酸、维生素B12水平明显低于对照组(P=0.01;P=0.005);颅内动脉瘤患者血浆Hcy水平与血清叶酸、维生素B12水平呈负相关(P＜0.05).多因素logistic回归分析显示:血浆Hcy是颅内动脉瘤发病的独立危险因素,比值比(OR)=3.961[P=0.019,95%可信区间(CI):1.255～12.500].结论 高Hcy血症与颅内动脉瘤发病有密切关系,可能是颅内动脉瘤发病的一个独立危险因素;血浆Hcy水平升高可能与血清叶酸、维生素B12水平降低有关.     

同型半胱氨酸与脑出血关系探讨

目的探讨脑出血与同型半胱氨酸（Hcy）的关系。方法选取脑出血患者58例，另选对照者60例，分别测定血浆Hcy、叶酸和维生素B12浓度。结果脑出血组的血浆Hcy水平较对照组明显升高，脑出血组Hcy与叶酸水平呈显著负相关，与VitB12水平呈负相关。结论高Hcy血症与脑出血呈正相关；血浆Hcy水平与叶酸、VitB12水平呈负相关。     

急性脑梗死患者血浆同型半胱氨酸、叶酸、维生素B12水平的测定及其临床意义

目的 探讨血浆同型半胱氨酸(Hcy)在急性脑梗死发病过程中的临床意义以及与病情、伴发症、叶酸、维生素B_(12)之间的关系。方法 采用化学发光法测定急性脑梗死患者血浆Hcy、叶酸、维生素B_(12)水平,并与对照组进行比较。结果急性脑梗死组血浆Hcy水平明显高于对照组(P<0.001),叶酸明显低于对照组(P<0.001);重型患者血浆Hcy水平明显高于中型及轻型患者(P<0.01,0.01),叶酸明显低于中型及轻型患者(P<0.01,0.05);伴发高血压病的患者血浆Hcy水平明显高于非高血压病的患者(P<0.05);急性脑梗死组血浆Hcy与叶酸、维生素B_(12)呈负相关(P<0.01,0.01);对照组血浆Hcy与叶酸呈负相关(P<0.05)。结论高Hcy血症是脑梗死的一个新的重要危险因素;Hcy水平与病情密切相关,与叶酸、维生素B_(12)呈负相关。     

左旋多巴对老年帕金森病患者血浆同型半胱氨酸水平的影响

目的观察左旋多巴对老年帕金森病(PD)患者血浆同型半胱氨酸(Hcy)、叶酸、维生素B12水平的影响。方法选择55例采用左旋多巴治疗的PD患者为观察组,另选择同时期健康体检者50例为对照组,分别测定观察组治疗前后及对照组的血浆Hcy、叶酸、维生素B12水平。结果观察组治疗后的血浆Hcy、维生素B12水平与治疗前及对照组比较,差异有统计学意义(P0.05);观察组治疗前后与对照组叶酸水平无显著差异(P0.05);回归分析显示,血浆Hcy与叶酸、维生素B12水平呈负相关(P0.05)。结论左旋多巴会提高帕金森病患者体内的血浆Hcy水平,及时补充叶酸、维生素B12利于降低患者体内血浆Hcy水平。     

高Hcy血症与急性缺血性脑卒中复发相关性研究

目的探讨血浆同型半胱氨酸(Hcy)水平与急性缺血性脑卒中复发的关系。方法将400例急性缺血性脑卒中患者按脑梗死类型分为动脉粥样硬化性血栓性梗死组(血栓组)、腔隙性脑梗死组(腔梗组)及心源性脑栓塞组(栓塞组),同时200例非急性卒中患者作为对照组,用荧光偏振免疫法(FPIA)测定血浆Hcy水平。并在发病后12个月对患者进行随访,确定有无梗死复发。研究患者血浆Hcy水平及1年脑梗死复发率之间的关系。结果 (1)血栓组、腔性脑梗死及栓塞组患者急性期血浆Hcy分别为16.93±11.46μmol.L-1、14.66±7.57μmol.L-1和16.58±8.72μmol.L-1,均高于对照组9.61±4.22μmol.L-1,P值均<0.001。各类型脑梗死患者之间Hcy无显著差异;(2)随访12个月血栓组、腔梗组及栓塞组的复发率分别为8.08%、7.05%和7.55%。各类型脑梗死患者复发率无显著差异;(3)高Hcy血症患者1年复发率11.68%,较非高Hcy血症患者的复发率(5.15%)高(P=0.022);(4)复发患者血浆Hcy水平(18.75±10.27μmol.L-1)高于无复发患者(14.57±8.50μmol.L-1,P=0.014);(5)多因素Logistic分析显示脑梗死复发与高血压(P=0.000)、糖尿病(P=0.000)、高Hcy血症有关(P=0.035)。结果缺血性脑卒中1年复发率与血浆Hcy升高有关,高Hcy血症是缺血性脑卒中复发的独立性危险因素。     

脑梗死患者血浆硫化氢、同型半胱氨酸、叶酸和维生素B6水平的改变及其相关性

目的 探讨脑梗死患者血浆硫化氢、同型半胱氨酸(Hcy)、叶酸和维生素B6水平的变化及其相关性.方法 检测60例脑梗死患者和40名正常对照者血浆硫化氢、Hcy、叶酸及维生素B6水平.脑梗死患者血浆硫化氢水平与Hcy、叶酸和维生素B6水平的相关性采用直线相关分析.结果 与正常对照组比较,脑梗死组血浆Hcy水平显著增高,血浆硫化氢、叶酸、维生素B6水平显著降低(P<0.05～0.001).血浆硫化氢水平与Hcy水平呈负相关(r=-0.6271,P<0.01),与叶酸及维生素B6水平呈正相关(r=0.5341,P<0.005;r=0.4615,P<0.05).结论 脑梗死患者血浆硫化氢、叶酸和维生素B6水平明显降低,Hcy水平升高.血浆低硫化氢水平可能参与了高Hcy血症致脑血管病的发病机制,可能是脑血管病的危险因素.     

血浆同型半胱氨酸水平与急性脑梗死关系探讨

目的 探讨血浆同型半胱氨酸(Hcy)水平与急性脑梗死的关系.方法 选择急性脑梗死患者80例为观察组,选取与之年龄、性别相匹配的同期我院健康体检者60例为对照组.所有入选者均清晨空腹抽取静脉血8 mL,分别送检血生化、叶酸(FA)、维生素B12 (VitB12)及血浆Hcy水平.结果 观察组血浆Hcy水平显著高于对照组(P＜0.01).观察组血浆Hcy水平与FA及VitB12水平均呈负相关.条件Logistic回归模型检验发现高Hcy血症的OR值5.268(95％ CI2.405～11.542).结论 高Hcy血症可能是急性脑梗死的独立危险因素.     

高同型半胱氨酸血症与脑梗死分层治疗之间的关系

目的探讨高同型半胱氨酸血症与脑梗死分层治疗的关系。方法选择脑梗死患者162例为梗死组,与病例组年龄、性别、种族等相匹配的未患过脑梗死健康体检者162例为对照组。采用高效液相色谱荧光检测法测定两组的血清Hcy水平。同时检测叶酸、维生素B12、血糖、血脂等。结果脑梗死血清Hcy水平显著高于对照组(P<0.01);血清叶酸及维生素B12水平与血清Hcy均成负相关;Logistic回归分析显示,高Hcy血症是脑梗死的独立危险因素(OR4.86595%CL1.902-8.443P<0.05),是脑梗死分层治疗须控制的危险因素。结论高同型半胱氨酸血症是脑梗死的独立危险因素,是分层治疗须控制的因素。     

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.     

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.     

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.     

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.     

Pediatric Epilepsy Surgery

Summary: The use of implantable arrays of epidural electrodes has made it possible to carry out extraoperative electrocorticography (ECoG) and functional localization in the awake child. This has permitted cortical excisions that are determined by criteria similar to those obtained during surgical procedures performed under local anesthesia in adults. In addition, the method also permits simultaneous ECoG and video monitoring during the child's symptomatic seizures, providing additional important localizing information that is impractical to obtain in operations under local anesthesia. We report our experience with 75 children, ages 5 months to 15 years, whom we have managed with epidural electrode arrays. The method of extraoperative ECoG is described and illustrative cases are presented to demonstrate its feasibility and utility in children. In addition, we call attention to gliomas as a common cause of chronic focal seizures in children. Of 49 children undergoing resection and followed for from 1 to 14 years (mean of 5.8 years), 32 (65%) are either seizure free or have had a significant reduction in seizure frequency that has unambiguously improved their quality of life. The results are analyzed further by relating the surgical outcome to each of the pathologic entities that caused the seizures. This analysis reveals the variety of neurological conditions that commonly cause intractable focal seizure disorder in children and distinguishes those pathologic entities in which the seizure disorder is apt to respond to surgical intervention from those that will not.     

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.