大剂量甲基强的松龙治疗外伤性弥漫性脑肿胀的疗效分析

目的 探讨大剂量甲基强的松龙(甲强龙)治疗外伤性弥漫性脑肿胀的疗效和安全性。方法 选择伤后12h内入院的外伤性弥漫性脑肿胀患者48例(实验组)接受大剂量甲强龙治疗,同期入院使用地塞米松(但未使用甲强龙治疗)的同类患者48例作对照组;所有患者其他治疗措施均基本相同。结果 将恢复良好、中残、重残合称为有效;将植物生存、死亡合称为无效。甲强龙实验组治疗有效19例(39.6％),无效29例(60.4％),有效组觉醒天数为17.8±5.3,d(n=19);对照组分别为10例(20.8％)及38例(79.2％),觉醒天数为24.7±7.4,d(n=10)。两组比较均有显著性差异(P<0.05或P相似文献   

早期大剂量纳洛酮治疗乙醇中毒合并颅脑损伤疗效分析

目的 探讨乙醇中毒合并颅脑损伤早期大剂量使用纳洛酮的临床治疗效果.方法 82例乙醇中毒合并颅脑损伤病人分成治疗组和对照组,各42例.治疗组早期给予大剂量纳洛酮,其余常规综合治疗2组相同.观察比较2组GCS、觉醒时间、血浆β-EP含量变化及预后情况.结果 治疗组在临床治疗有效率、觉醒时间、GCS变化上较对照组有显著差异(P<0.05),且与对照组相比血浆β-EP含量下降极其显著(P<0.01).结论 早期大剂量纳洛酮治疗乙醇中毒合并颅脑损伤可缩短昏迷时间,促进病人神经功能恢复.纳洛酮使用安全,未见毒副作用.     

纳络酮治疗重型颅脑损伤病人的疗效观察

目的观察重型颅脑损伤病人不同时期使用纳洛酮对预后的影响。方法重型颅脑损伤病人41例分为早期治疗组(伤后12h内足量或大剂量使用纳洛酮)12例,晚期治疗组(伤后7～10d使用纳洛酮)14例,对照组15例,比较观察各组病人的疗效。结果早期治疗组较晚期治疗组、对照组的意识复苏时间明显缩短(P<0.05),拔气管导管时间明显提前(P<0.01),肺部感染率则无明显差别(P>0.05);晚期治疗组与对照组上述各项指标则无显著差异(P>0.05)。结论早期足量或大剂量使用阿片受体阻滞剂纳洛酮能明显减轻重型颅脑损伤病人的继发损伤,缩短意识复苏时间及气管导管滞留时间。     

大剂量白蛋白治疗弥漫性轴索损伤36例疗效观察

目的 探讨大剂量白蛋白对弥漫性轴索损伤(DAI)患者的临床治疗作用。方法 大剂量白蛋白治疗DAI36例与同等 条件下未用大剂量白蛋白的患者39例进行比较。结果 实验组觉醒天数为(30.80±2.36)d,对照组为(46.60±6.78)d,两组比较差 异显著(P<0.05)。实验组恢复良好11例(30.5％),死亡9例(25.0％);对照组分别为6例(15.3％)及15例(38.5％),两组比较均差 异显著(P<0.05)。实验组血液流变学4项指标较对照组下降明显(P<0.05)。结论 DAI早期应用大剂量白蛋白治疗可降低死亡 率,提高良好率,缩短昏迷时间。     

大剂量纳洛酮治疗急性脑梗死临床研究

目的 观察早期应用大剂量纳洛酮对脑梗死治疗的有效性及安全性.方法 106例脑梗死患者随机分成大剂量纳洛酮治疗组(n=54)和常规剂量纳洛酮对照组(n=52),治疗组给予纳洛酮4mg/d,而对照组1.2mg/d,2周一疗程,进行神经功能缺损评分,观察症状改善时间.结果 治疗组神经功能改善,总有效率88.89%,明显高于对照组的73.07%(P<0.05),而且治疗组24h内症状改善24.07%,明显好于对照组的13.46%(P<0.05).结论 早期大剂量纳洛酮治疗急性脑梗死,能显著减轻神经功能损伤而且无明显不良反应.     

高压氧治疗重型颅脑损伤的疗效分析

目的观察高压氧对重型颅脑损伤的治疗效果,并分析其作用机制。方法80例重型颅脑损伤患者随机分为高压氧治疗组(n=40)和对照组(n=40),观察两组患者的清醒人数,清醒时间,GCS评分的变化,治疗3个月后GOS评分、病死和植物状态比例,并分析两组的临床疗效,同时监测治疗前后脑动脉血流速度变化。结果治疗组的清醒人数的比例明显高于对照组(P<0.05),觉醒平均时间较对照组明显缩短(P<0.05),3疗程后GCS评分和3个月后的GOS评分明显高于对照组(P<0.05)、植物状态及死亡率较对照组低(P<0.05)、治愈率及总有效率明显高于对照组(P<0.01);治疗组2个疗程后血流速度较对照组下降明显(P<0.05)。结论早期行高压氧治疗对重型颅脑损伤具有明显疗效,可能与高压氧能有效提高血氧含量、扩大血氧弥散半径、促进血管生成和侧枝循环建立、有效缓解脑血管痉挛状态、清除自由基、减少缺血区脑细胞凋亡等作用有关。     

重型颅脑损伤继发性脑水肿液体疗法的应用再探讨

目的探讨重型颅脑损伤继发性脑水肿的补液方法。方法选取我院收治的重型颅脑损伤继发性脑水肿病人44例,随机分为实验组(24例)和对照组(20例),进行对比研究。实验组不限水、钠入量,按需补入,同时给予扩容治疗;对照组限水、钠入量,使病人处于轻度的脱水状态。结果伤后1月根据GOS分级,实验组在死亡率、恢复良好率方面均优于对照组(P<0.05);实验组GCS评分于伤后1周即与对照组有显著性差异(P<0.01);同时实验组血液粘滞度改善较快。结论重型颅脑损伤继发性脑水肿采用个体化补液,适当扩容,能起到促进病人恢复、降低致残率及死亡率等作用。     

局部亚低温联合尼莫地平防治重型颅脑损伤术后脑血管痉挛的疗效研究

目的:观察脑部亚低温联合尼莫地平防治重型颅脑损伤患者术后脑血管痉挛(CVS)的疗效及临床预后.方法:入选103例创伤性重型颅脑损伤患者为研究对象,据随机数字表分为观察组(53例)和对照组(50例),对照组患者术后给予局部亚低温(34～35℃)实施脑保护3～5 d,观察组在同对照组治疗的基础上24 h静脉泵注尼莫地平注射液,起始速率0.5 mg/h,最大速率2 mg/h,连续14 d,其间每日监测大脑中动脉平均血流速度(VMCA),判定CVS严重程度,术后6个月判定颅脑损伤预后.结果:观察组术后的VMCA 3 d时为(95.8±17.2) mL/s、5d时为(89.5±16.3)mL/s、7d时为(83.7±15.8)mL/s、14 d时为(76.6±10.2)mL/s均明显低于对照组水平,相应为(108.5±21.7)mL/s、(101.2±18.5)mL/s、(92.8±19.7)mL/s、(84.2±13.9) mL/s(P＜0.05).观察组术后CVS发生率明显低于对照组(15.1％ vs 32.0％)(x2 =4.114,P=0.043),两组术后CVS的发生程度构成差异显著(Z=-2.150,P=0.032).观察组住院期间病死率低于对照组(7.5％ vs 18.0％)(x2=2.549,P=0.110);术后6个月,观察组颅脑功能达到良好的比例高于对照组(58.5％ vs 44.0％),伤残率低于对照组(32.1％vs 38.0％),差异均无统计学意义(x2=2.163,P=0.145;x2 =0.397,P=0.529).结论:重型颅脑损伤患者术后在实施脑部亚低温支持的基础上,联合静脉泵注尼莫地平注射液,能进一步平抑颅脑损伤后急性高灌注,降低CVS的发生率及严重程度,表现出改善远期预后的趋势.     

高温高湿环境下重型颅脑损伤的临床特点分析

目的探讨高温高湿环境下重型颅脑伤的临床特点,降低死残率。方法从中国人民解放军第422医院数据库中随机抽取高温高湿环境下(气温≥35℃,相对湿度≥80%)重型颅脑损伤患者500例为高温高湿组,非高温高湿环境下(气温,27.42℃±1.37℃,相对湿度50.25%±6.74%)重型颅脑损伤患者500例为对照组。二组病人治疗方法相同,对二组病人觉醒天数、并发症、后遗症和预后进行统计分析。结果高温高湿组死亡率为42%,对照组为30%,高温高湿组觉醒天数、并发症、后遗症和死残率比对照组明显高(P<0.01)。结论高温高湿环境下重型颅脑损伤的主要临床特点是较非高温高湿环境下病人继发性脑损伤更严重;生命体征紊乱明显;脑水肿更严重;伴其它主要器官损伤更严重;癫痫发病率高以及预后更差。     

重型颅脑损伤病人颅内压变化及纳洛酮的治疗作用

目的观察重型颅脑损伤患者颅内压变化及大剂量纳洛酮的治疗效果。方法选择重型脑损伤患者（GCS计分3—8分）82例。随机分治疗组42例,除采用临床综合治疗外并应用大剂量纳洛酮;对照组仅采用临床综合治疗,监测颅内压及常规临床监护,观察病人预后。结果重症颅脑外伤病人颅内压增高明显,颅内压．急剧升高与死亡率明显相关。纳洛酮治疗组颅内压明显低于对照组,预后较对照组好,并发症少。结论重症颅脑外伤颅内压水平与病人预后明显相关。大剂量纳洛酮能够改善重症颅脑损伤引起的脑水肿、高颅压,进而改善脑组织缺氧,改善病人预后。     

Denervation study of synapses of organ of corti of old world monkeys

Fine structural characteristics of synapses in the spiral organ of Corti were examined, with reference to differences between inner and outer haircell systems, and to location of neurons of origin of efferent axons. Surgical interruption of crossed olivocochlear bundle, of vestibular nerve, of facial nerve, and excision of superior cervical ganglia were used to determine the pathways of efferent axons. Interruption of the vestibular nerve near the brainstem results in degeneration of all efferent terminals on outer hair cells. Mid-line lesions at, and caudal to, the facial colliculus result in degeneration of about half of these efferent terminals. Efferent synaptic bulbs to the inner hair-cell system are small, of the order of one micron, and form type 2 junctions with afferent dendrites. They tend to have more large dense-core vesicles (about 80 nm) than the large efferent terminals of the outer hair-cell system, and appear to be the terminals of axons in the habenula perforata, which exhibit varicosities laden with large dense core vesicles. The varicosities are unaffected by excision of the superior cervical ganglia. So far as our material can reveal, it appears that the varicosities in the habenula perforata do not survive vestibular root interruption, nor do the efferent processes in the internal spiral bundle or at the base of inner hair cells. Most interestingly, the afferent processes of the inner hair-cell system, as identified for example by their relation to pre-synaptic bodies in the inner hair cells, are subject to a trans-synaptic reaction after severance of the vestibular root. They undergo a dramatic cytological transformation, characterized by increase of volume, engorgement with microtubules, microfilaments, microvesicles of various sizes, and clusters of lysosomes. Thus, both the efferent and afferent terminals of the inner hair-cell system show marked cytological differences from the corresponding terminals of the outer hair cell system.     

Mechanism of action of tubocurarine on nicotinic cholinoreceptors of neurons of the sympathetic ganglia of rats

Tubocurarine (Tc) effect on membrane currents elicited by acetylcholine (ACh) was studied in isolated superior cervical ganglion neurons of rat using patch-clamp method in the whole-cell recording mode. The "use-dependent" block of ACh current by Tc was revealed in the experiments with ACh applications, indicating that Tc blocked the channels opened by ACh. Mean lifetime of Tc-open channel complex, tau, was found to be 9.8 +/- 0.5 s (n = 7) at -50 mV and 20-24 degrees C. tau exponentially increased with membrane hyperpolarization (e-fold change in tau corresponded to the membrane potential shift by 61 mV). Inhibition of the ACh-induced current by Tc (3-30 microM/1) was completely abolished by membrane depolarization to the level of 80-100 mV. Inhibition of ACh-induced current was augmented at increased ACh doses. It is concluded that the open channel block produced by Tc is likely to be the only mechanism for Tc action on nicotinic acetylcholine receptors in superior cervical ganglion neurons of rat.     

The effect of age of onset of PD on risk of dementia

Background Dementia occurs in the majority of patients with Parkinson’s disease (PD). Late onset of PD has been reported to be associated with a higher risk for dementia. However, age at onset (AAO) and age at baseline assessment are often correlated. The aim of this study was to explore whether AAO of PD symptoms is a risk factor for dementia independent of the general effect of age. Methods Two community-based studies of PD in New York (n = 281) and Rogaland county, Norway (n = 227) and two population-based groups of healthy elderly from New York (n = 180) and Odense, Denmark (n = 2414) were followed prospectively for 3–4 years and assessed for dementia according to DSM-IIIR. All PD and control cases underwent neurological examination and were followed with neurological and neuropsychological assessments. We used Cox proportional hazards regression based on three different time scales to explore the effect of AAO of PD on risk of dementia, adjusting for age at baseline and other demographic and clinical variables. Findings In both PD groups and in the pooled analyses, there was a significant effect of age at baseline assessment on the time to develop dementia, but there was no effect of AAO independent of age itself. Consistent with these results, there was no increased relative effect of age on the time to develop dementia in PD cases compared with controls. Interpretation This study shows that it is the general effect of age, rather than AAO that is associated with incident dementia in subjects with PD. Received in revised form: 22 December 2005     

Limits of deinstitutionalization--perspectives of relatives of psychiatric patients

After a hopeful beginning, the social process of the reintegration of those with severe mental illness has come to a standstill. I am led to wonder whether "the community" really wants to live together with people suffering from severe mental illness, and if so, how closely? As long as the medical treatment of mental illness provided by the general practitioners is fundamentally deficient, as they are not able to prescribe the necessary interventions--such as out-patient psychiatric nursing, and service providers in the out-patient sector are content with offering increasingly intensive forms of care for the less seriously ill at the cost of the Social Welfare System--the reintegration of those with serious mental illness remains an illusion--which is mainly to the benefit of providers of residential care in homes and hostels.