正确掌握癫癎外科治疗的时机和术式

据中国最新的流行病学调查，癫痫终生患病率为7．0‰，活动性癫痫患病率(5年内有发作)为4．9‰。70％～80％的癫痫患者经过正规的内科治疗，可以得到控制或缓解，但20％～30％为难治性癫痫患者，即难治性癫痫患者在我国不少于100万例：对于部分癫痫患者，适宜的手术治疗能够减轻、减少发作，并有机会完全控制。现在，国内的癫痫手术治疗正蓬勃开展，并且取得了一定的良好成果，但还存在着明显的不足。对于现阶段的癫痫手术治疗．亟需规范化、标准化。癫痫手术涉及了手术时机的掌握、综合定位以及合理术式的选择，其中手术时机掌握谈论较少。     

基诺族精神病、精神发育迟滞和癫痫的10年随访调查

对基诺族精神病、精神发育迟滞和癫痫进行１０年随访。精神病终身患病率前后为４．０３‰，３．８５‰，现患病率为２．８８‰，２．８８‰。精神病平均年发病率为９．６１／１０万人口。精神分裂症的现患病率前后为２．４２‰，２．４０‰，男性明显高于女性。随访表明，精神分裂症在自然状态下预后很差，社会性结局不好。精神发育迟滞现患病率前后为１．８４‰，２．９８‰，平均年发病率为１５．３８／１０万人口。癫痫（大发作）现患病率前后为１．６１‰，１．３５‰。结果提示，在自然状态下癫痫的预后很差。     

海南省老年期痴呆的流行学调查

本调查６０岁及以上人群２５２８２人，查出痴呆病例１５例，老年期痴呆患为５．９３‰，与１２地区和北京西城区结果相类似，但远低于上海高氏结果４２．１‰。仅有２０％病例曾接受治疗，多数病例缺乏医疗保健条件。     

特发性癫痫与癫痫基因的研究进展

特发性癫痫与癫痫基因的研究进展郎森阳癫痫是神经系统疾病中较常见的一组慢性脑功能异常征候群，其患病率在发达国家为总人口数的１．０‰［１］，在我国部分地区为３．５‰～４．８‰［２］。特发性癫痫是一大类具有家族遗传倾向的全身发作性癫痫，约占各种类型癫痫患者...     

基诺族精神病,精神发育迟滞和癫痫的10年随访调查

对基诺族精神病、精神发育迟滞和癫痫进行１０年随访。精神病终身患病率前后为４．０３‰，３．８５‰，现患病率为２．８８‰，２．８８‰。精神病平均年发病率为９．６１／１０万人口。精神分裂症的现患病率前后为２．４２‰，２．４０‰，男性明显高于女性。随访表明，精神分裂症在自然状态下预后很差，社会性结局不好。精神发育迟滞现患病率前后为１．８４‰，２．９８‰，平均年发病率为１５．３８／１０万人口。癫痫（大发作）     

河南焦作市武陟县农村人群癫痫流行病学调查

目的：调查了解我国农村地区癫痫的患病率及治疗缺口，为开展防治工作提供依据。方法：河南省焦作市武陟县作为调查点，采用随机整群抽样方法确定调查人群，由经过统一培训的医生入户调查。调查人数为12457人。凡初筛调查时确诊或可疑的癫痫患者，均经神经科医生再次访查确诊。结果：调查确诊59例癫痫患者，患病率为4．7‰。活动性癫痫患病率为3．5‰，年发病率32．1／10万人口。全部患者中有25．4％未治疗，47．5％患者治疗不正规。活动性癫痫的治疗缺口为32．5％。结论：本次调查农村地区癫痫患病率与以往报道接近，约有2／3患者没有得到正确治疗，应尽快制订合理的干预对策。     

干细胞移植治疗癫痫的最新研究进展

据WHO报道，世界范围内癫痫患病率为3‰-7‰。在我国的患病率约为7‰，约有1000余万患者，且多数为部分性发作，而部分性发作中又以颞叶癫痫最为多见。 1病理机制 目前主要认为是海马硬化，     

病灶切除与热灼联合术在难治性癫痫治疗中的应用

目的 研究病灶切除与热灼联合手术方法治疗继发性、难治性癫痫的临床效果。方法 对291例继发性、难治性癫痫患采取病灶切除与热灼联合手术的治疗方法，并随访观察此种联合手术方法对难治性癫痫的控制效果：结果 采用病灶切除与热灼联合手术后，291例患中，有211例(72．5％)发作消失，有50例(17．2％)发作减少50％以上，对癫痫总的有效控制率为89．7％，随访1．5～4．0年，平均23个月，211例发作消失的患中有83例(39．3％)已停服抗癫痫药；同时，病灶切除与热灼联合术无永久性的术后并发症：结论 病灶切除与热灼联合术治疗继发性、难治性癫痫，安全并且治疗效果令人满意。     

家庭背景与社会支持对癫痫患者生活的影响

目的：调查家境背景对癫痫病人的影响和社会对癫痫病人的支持程度。方法：病人来源于汕头地区三家综合医院门诊，随机取样。由检查直接询问病人和他们的亲属，对200例癫痫患及家庭和200例正常人及家庭对癫痫病人的看法与支持的程度等进行了调查。用SPSS8．0软件统计，结果：病人组患和父母的化程度，职业和经济收入明显低于对照组，P＜0．010。生活条件如，燃料，饮水，居住条件都低于对照组，而医药费的支出很大，P＜0．0000。结论：结果显示癫痫病人父母低化直接影响着病人的发病，治疗，教育，职业和经济收入，也是导致贫困和生活质量低的主要原因，在社会支持度方面，病人缺乏理解，同情与支持。     

血药浓度监测对成人癫痫患者生活质量的影响

目的 观察血药浓度监测对成人癫痫患生活质量的影响。方法 用前瞻性、自身对照的方法对长期服用抗癫痫药治疗效果不佳的成人癫痫患进行了血药浓度和生活质量的评定，观察其药物影响的特点。结果 (1)患组与对照组相比生活质量方面差别具有非常显性意义(P＜0．01)；(2)有效治疗浓度范围内急生活质量提高，差别有显性意义(P＜0．05)；(3)血药浓度与生活质量间具有显正相关(P＜0．01)。结论 成人癫痫患存在生活质量下降，合理用药、血药浓度监测可控制癫痫发作、提高患生活质量。     

视频脑电图在小儿癫痫诊断中的应用

目的评价视频脑电图(video-EEG)在小儿癫诊断中的应用价值。方法对126例具有发作性症状的患儿进行连续8h的包括清醒、睡眠、诱发试验及必要的认知测验的视频脑电图监测。结果经发作期视频脑电图证实,39例初诊为癫性发作的患儿中14例(35%)为非癫性发作;15例其他症状发作中13例(86%)为非癫性发作。64例样放电患儿中51例(80%)确定发作类型,22例(34%)确定癫类型。视频脑电图可发现短暂轻微的癫发作及样放电引起的一过性认知损伤。结论视频脑电图在排除非癫性发作、确定癫性发作的类型、评价脑电-临床关系方面可提供准确可靠的证据,进一步提高癫的临床诊断水平。     

Role of glutathione in repair of free radical damage in hippocampus in vitro.

Depletion of glutathione (GSH), an intrinsic antioxidant, increases vulnerability to free radical damage in a number of cell systems. This study investigates the role of GSH in limiting electrophysiological damage and/or recovery from free radical exposure in slices of guinea pig hippocampus. Synaptic potentials (PSPs) and population spikes (PSs) were recorded from field CA1. Free radicals were generated from 0.006% peroxide through the Fenton reaction. Analysis of the input-output curves showed that peroxide treatment decreased PSPs and impaired ability of the PSPs to generate PSs as previously reported. Recovery was nearly total within a half hour. Treatment with 5 mM buthionine sulfoximine (BSO) for 2 h depleted hippocampal GSH to 79.2% of control values. The extent of free radical damage was not increased. Recovery, however, was only partial. GSH was further depleted by oxidation with diamide or covalent bonding with dimethyl fumarate (DMF) immediately before and during the peroxide treatment. Neither diamide nor DMF treatment in BSO-incubated tissue enhanced peroxide-induced electrophysiological deficits. Following these treatments, however, tissue showed little recovery from free radical damage. We conclude that glutathione is essential for repair processes in hippocampal neurons exposed to oxidative damage.     

Neuroprotective properties of memantine in different in vitro and in vivo models of excitotoxicity

The pathogenesis of stroke, trauma and chronic degenerative diseases, such as Alzheimer's disease (AD), has been linked to excitotoxic processes due to inappropriate stimulation of the N-methyl-D-aspartate receptor (NMDA-R). Attempts to use potent competitive NMDA-R antagonists as neuroprotectants have shown serious side-effects in patients. As an alternative approach, we were interested in the anti-excitotoxic properties of memantine, a well-tolerated low affinity uncompetitive NMDA-R antagonist presently used as an anti-dementia agent. We explored in a series of models of increasing complexity, whether this voltage-dependent channel blocker had neuroprotective properties at clinically relevant concentrations. As expected, memantine protected neurons in organotypic hippocampal slices or dissociated cultures from direct NMDA-induced excitotoxicity. However, low concentrations of memantine were also effective in neuronal (cortical neurons and cerebellar granule cells) stress models dependent on endogenous glutamate stimulation and mitochondrial stress, i.e. exposure to hypoxia, the mitochondrial toxin 1-methyl-4-phenylpyridinium (MPP+) or a nitric oxide (NO) donor. Furthermore, memantine reduced lethality and brain damage in vivo in a model of neonatal hypoxia-ischemia (HI). Finally, we investigated functional rescue (neuronal capacity to migrate along radial glia) by memantine in cerebellar microexplant cultures exposed to the indirect excitotoxin 3-nitropropionic acid (3-NP). Potent NMDA-R antagonists, such as (+)MK-801, are known to block neuronal migration in microexplant cultures. Interestingly, memantine significantly restored the number of neurons able to migrate out of the stressed microexplants. These findings suggest that inhibition of the NMDA-R by memantine is sufficient to block excitotoxicity, while still allowing some degree of signalling.     

Storage of lipofuscin in neurons in mucopolysaccharidosis

Summary A histochemical and ultrastructural study was made on the brain of a 23-year-old man with Sanfilippo's syndrome. In accordance with previous reports the cortical nerve cells contained a PAS-positive lipid storage substance. This showed intense autofluorescence in UV-light and was positive with various stains for lipofuscin. The storage material appeared ultrastructurally as inclusion bodies composed of short lamellated membranes, granular material, and vacuoles. In addition, concentrically and transversely lamellated membranous cytoplasmic bodies were observed in the nerve cells. It is concluded that the PAS-positive lipid storage material in the neurons was composed partly of lipofuscin in addition to other lipids presumably glycosphingolipids.Supported by a grant from the Expressen Prenatal Research Foundation