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Epilepsy research. Supplement最新文献

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Substantia nigra GABA receptors can mediate anticonvulsant or proconvulsant effects. 黑质GABA受体可介导抗惊厥或前惊厥作用。
Pub Date : 1996-01-01
S L Moshé, D S Garant
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引用次数: 0
Possible mechanisms of seizure-related cell damage in the dentate hilus. 齿状门癫痫相关细胞损伤的可能机制。
Pub Date : 1996-01-01
P A Schwartzkroin, P S Buckmaster, B W Strowbridge, D D Kunkel, J Owens, J Pokorný
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引用次数: 0
Seizure-induced molecular changes, sprouting and synaptogenesis of hippocampal mossy fibers. 癫痫诱导海马苔藓纤维的分子变化、发芽和突触发生。
Pub Date : 1996-01-01
H Pollard, K Bugra, M Khrestchatisky, A Represa, Y Ben-Ari
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引用次数: 0
The relationship between seizures and damage in the maturing brain. 癫痫发作与成熟大脑损伤之间的关系。
Pub Date : 1996-01-01
E F Sperber
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引用次数: 0
Severe seizures in young children are associated with hippocampal neuron losses and aberrant mossy fiber sprouting during fascia dentata postnatal development. 幼儿严重癫痫发作与出生后牙筋膜发育过程中海马神经元丢失和苔藓纤维异常萌发有关。
Pub Date : 1996-01-01
G W Mathern, J P Leite, J K Pretorius, B Quinn, W J Peacock, T L Babb
{"title":"Severe seizures in young children are associated with hippocampal neuron losses and aberrant mossy fiber sprouting during fascia dentata postnatal development.","authors":"G W Mathern, J P Leite, J K Pretorius, B Quinn, W J Peacock, T L Babb","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77115,"journal":{"name":"Epilepsy research. Supplement","volume":"12 ","pages":"33-43"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20244070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
NMDA and non-NMDA synaptic currents in rat neocortex during early postnatal development. 出生后早期大鼠新皮层的NMDA和非NMDA突触电流。
Pub Date : 1996-01-01
J J Hablitz, E C Burgard
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引用次数: 0
Genomic structure, sequence, and physiological expression of mKv 1.5, a mouse potassium channel gene. 小鼠钾通道基因mKv 1.5的基因组结构、序列和生理表达。
Pub Date : 1996-01-01
V A Street, W F Hopkins, B L Tempel
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引用次数: 0
Use of rational polypharmacy to treat epilepsy. 合理综合用药治疗癫痫的应用。
Pub Date : 1996-01-01
J A Ferrendelli
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引用次数: 0
Definition of rational antiepileptic polypharmacy. 合理抗癫痫复方药的定义。
Pub Date : 1996-01-01
B J Wilder, R W Homan

Rational polypharmacy is in its earliest stages of development and will require substantial additional development to realize its full potential. Indeed, despite the powerful appeal of the concept, clinical proof is not yet available that RP is superior to monotherapy. Important questions need to be addressed: 1. Will RP control seizures more effectively than monotherapy? 2. What data are needed to develop RP for a specific patient? 3. Will RP be cost effective? 4. Can RP be developed which will treat or prevent epilepsy while controlling seizures? Possible approaches to these questions could include: 1. The development of a data base for prospective use to monitor patients being treated at Epilepsy Centers using RP principles. 2. Use the data obtained from the above to construct more specific studies to compare identified combination therapies with monotherapy. 3. Prospectively compare in a placebo controlled, blinded study, the effect of the combination of an anti-ictal medication and a laboratory proven antiepileptic drug for prevention of the development of epilepsy in an at risk population such as head trauma or stroke.

理性多药疗法还处于发展的早期阶段,需要大量的额外发展才能充分发挥其潜力。事实上,尽管这一概念具有强大的吸引力,但临床证据尚未表明RP优于单一疗法。需要解决的重要问题:1。RP是否比单一疗法更有效地控制癫痫发作?2. 需要哪些数据来开发针对特定患者的RP ?3.RP是否具有成本效益?4. RP能否在控制癫痫发作的同时治疗或预防癫痫?回答这些问题的可能方法包括:1。开发一个数据库,用于使用RP原则监测癫痫中心接受治疗的患者。2. 利用上述数据构建更具体的研究,比较已确定的联合治疗与单一治疗。3.在一项安慰剂对照的盲法研究中,前瞻性地比较了抗癫痫药物和实验室证实的抗癫痫药物联合使用对高危人群(如头部创伤或中风)预防癫痫发展的效果。
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引用次数: 0
Is there a mechanistic basis for rational polypharmacy? 合理的多药疗法有机制基础吗?
Pub Date : 1996-01-01
R L Macdonald

Established antiepileptic drugs (AEDs) decrease membrane excitability by interacting with neurotransmitter receptors or ion channels. AEDs developed prior to 1980 appear to act on sodium channels. gamma-amino butyric acid type A (GABAA) receptors (GABARs) or calcium channels. Benzodiazepines and barbiturates enhance GABAR-mediated inhibition. Phenytion, carbamazepine and possibly sodium valproate decrease high-frequency repetitive firing of action potentials by enhancing sodium channel inactivation. Ethosuximide and sodium valproate reduce a low threshold (T-type) calcium channel current. The mechanisms of action of the new AEDs are not fully established. Gabapentin binds to a high affinity site on neuronal membranes in a restricted regional distribution of the central nervous system. This binding site may be related to a possible active transport process of gabapentin into neurons; however, this has not been proven and the mechanism of action of gabapentin remains uncertain. Lamotrigine decreases sustained high-frequency repetitive firing of voltage-dependent sodium actin potentials that may result in a preferential decreased release of presynaptic glutamate. Oxcarbazepine's mechanism of action is not known; however, its similarity in structure and clinical efficacy to that of carbamazepine suggests that its mechanism of action may involve inhibition of sustained high-frequency repetitive firing of voltage-dependent sodium action potentials. Vigabatrin irreversibly inhibits GABA transaminase, the enzyme that degrades GABA, thereby producing greater available pools of presynaptic GABA for release in central synapses. Increased activity of GABA at postsynaptic receptors may underlie the clinical efficacy of vigabatrin. The potential mechanistic bases for rational polypharmacy are reviewed.

已有的抗癫痫药物通过与神经递质受体或离子通道相互作用来降低膜的兴奋性。1980年以前研制的aed似乎对钠离子通道起作用。γ -氨基丁酸A型(GABAA)受体(gabar)或钙通道。苯二氮卓类药物和巴比妥类药物增强gabar介导的抑制作用。Phenytion,卡马西平和可能的丙戊酸钠通过增强钠通道失活来减少动作电位的高频重复放电。乙氧亚胺和丙戊酸钠降低低阈值(t型)钙通道电流。新型抗癫痫药的作用机制尚未完全确定。加巴喷丁在中枢神经系统的有限区域分布中与神经元膜上的高亲和力位点结合。该结合位点可能与加巴喷丁进入神经元的主动转运过程有关;然而,这一点尚未得到证实,加巴喷丁的作用机制仍不确定。拉莫三嗪减少持续高频重复放电的电压依赖性肌动蛋白钠电位,可能导致优先减少释放突触前谷氨酸。奥卡西平的作用机制尚不清楚;然而,其结构和临床疗效与卡马西平相似,表明其作用机制可能涉及抑制电压依赖性钠动作电位的持续高频重复放电。Vigabatrin不可逆地抑制GABA转氨酶(一种降解GABA的酶),从而产生更多的突触前GABA供中央突触释放。突触后受体GABA活性的增加可能是维加巴林临床疗效的基础。综述了合理多药的潜在机制基础。
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引用次数: 0
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Epilepsy research. Supplement
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