改良丁丙诺啡法戒毒临床观察

目的：了解改良丁丙诺啡方法对海洛因依赖者戒毒的疗效。方法：对海洛因信赖者戒毒治疗的病人９０例分为２组,Ａ组以氯氮平、氯羟安定治疗;Ｂ组以氯氮平、氯羟安定联用丁丙诺啡治疗。比较两组的疗效、戒断症状及药物副作用的差异。结果：两种治疗方案对海洛因信赖者戒毒治疗均有效,但改良丁丙诺啡组患者戒断症状轻,用药量较小,两组间有显著性差异。结论：改良丁丙诺啡组对戒断症状的控制优于单独使用氯氮平和氯羟安定组,治疗安     

丁丙诺啡与美沙酮对鸦片依赖者的维持治疗

丁丙诺啡与美沙酮对鸦片依赖者的维持治疗【英】／ＫｏｓｔｅｎＴＲＪＮｅｒｖＭｅｎｔＤｉｓ－１９９３，１８１（６）；－３５８～３６４丁丙诺啡已替代美沙酮维持治疗鸦片依赖者。但是门诊病人维持治疗的最小剂量尚未确定。每日２～３ｍｇ舌下含服进行脱瘾的研究，显示...     

美沙酮联用丁丙诺啡对海洛因依赖重度药瘾戒毒治疗临床研究

目的　探索对海洛因依赖重度药瘾较理想的戒毒治疗方法。　　方法　采用美沙酮与丁丙诺啡联合用药方案 ,对海洛因依赖重度药瘾 41例行戒毒治疗 ,1 2天为一疗程 ,并与单用美沙酮组 2 0例进行比较。　　结果　联合用药组控制症状较彻底 ,鸦片类药物戒断症状量表 (OWS)总分平稳下降 ,症状波动小 ,减药顺利 ,两药替换平稳 ,戒毒成功率 73 2 %。　　结论　我们认为美沙酮联用丁丙诺啡是一种值得推荐的戒毒治疗方法。     

海洛因依赖者脱瘾治疗中丁丙诺啡与美沙酮的比较研究

美沙酮(methadone)系目前世界上广泛用于阿片类药物依赖脱瘾(detoxification)治疗的经典药物。治疗方案有10天和21天替代递减法等多种。21天递减法有替代递减顺利、戒断症状较轻、给药方便、易于接受等优点,但脱瘾时间相对较长。丁丙诺啡(buprenorphine)理论上可用于阿片类药物依赖的替代治疗和脱瘾。并能抑制海洛因依赖者使用海洛因和有强化作用。目前美     

盐酸丁丙诺啡治疗海洛因依赖临床观察

85例海洛因依赖采用盐酸丁内诺啡注射液递减法戒毒的临床效果表明，60例完成治疗过程，效果良好，25例脱试。平均住院19.5天，盐酸丁丙诺啡人均用量9.45mg。9天内快速递减后，戒断症状控制好，副作用小，使用方便。     

丁丙诺啡替代海洛因脱毒治疗50例临床报告

丁丙诺啡是兼具对Ｍ受体和Ｋ受体的激动作用和拮抗特性的阿片类化合物。它的激动活性可用来替代海洛因脱毒治疗，其拮抗活性决定了它的依赖性，但比纯激动剂明显较轻，是具有应用价值的戒毒药物［１］。现将我们近期用丁丙诺啡治疗５０例脱瘾病例报告如下。１资料与方法１...     

美沙酮与丁丙诺啡治疗海洛因依赖临床疗效观察

应用美沙酮、丁丙诺啡替代递减疗法治疗100例海洛因依赖患者。采用随机开放临床试验，分两组对照观察。结果显示：美沙酮控制戒断症状疗效显著，作用时间长，经济方便，患者易接受，安全性更高。     

布比卡因联合丁丙诺啡在臂丛神经阻滞麻醉中的效果分析

目的观察布比卡因联合丁丙诺啡在臂丛神经阻滞麻醉中的效果。方法将80例行臂丛神经阻滞麻醉患者随机分为对照组与联合组,每组40例,均采取肌间沟径路阻滞。对照组用药:0.75%布比卡因注射液15mL加0.9%氯化钠溶液15mL;联合组用药:在对照组用药内加入丁丙诺啡注射液0.075mg。比较2组患者生命体征变化、麻醉起效时间和维持时间、术后镇痛效果及不良反应。结果 2组患者的生命体征变化和不良反应比较,差异无统计学意义(P>0.05);联合组麻醉起效时间较对照组明显缩短,麻醉维持时间及术后镇痛维持时间均长于对照组,差异有统计学意义(P<0.05)。结论在臂丛神经阻滞麻醉中,丁丙诺啡可加强布比卡因的麻醉效果,缩短布比卡因的起效时间,而且安全。     

综合治疗周围面神经麻痹的疗效观察

目的 探讨周围性面神经麻痹的最佳治疗方法。方法 对48例周围性面神经麻痹的患者的发病早期（1周内）采用药物、物理、康复综合性治疗。结果 完全性周围性面神经麻痹的治疗有效率为86％。不完全性周围性麻痹的有效率为97％，总有效率为94％。两个疗程的有效率为88％，三个疗程的有效率为100％。结论 采用综合治疗周围性面神经麻痹能迅速改善症状。缩短痛程，显效率明显提高，一般以三个疗程为宜，老年人有伴发病者可适当延长治疗时间。     

不同疗程甘露醇对急性脑出血患者疗效的影响

目的 观察不同疗程甘露醇对急性脑出血患者的疗效影响。方法 应用２０％甘露醇治疗急性脑出血患者１６３例，观察组８５例，疗程３０天，对照组７８例，疗程１０天，在治疗前、治疗后１０天、３０天、９０天分别进行改良爱丁堡－斯堪的那维亚评分（ＭＥＳＳＳ），在３０天、９０天加用日常生活能力评价（ＡＤＬ）。结果 两组在治疗后１０天的显效率、总有效率比较无显著差异（Ｐ〉０．０５），在治疗后３０天比较有显著差异（Ｐ〈     

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.     

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     

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.