蛛网膜下腔出血钠代谢失衡的临床分析

目的分析蛛网膜下腔出血钠代谢失衡的原因、特点、处理方法及对预后的影响。方法回顾性分析58例蛛网膜下腔出血患者并发钠代谢紊乱的临床资料。结果低钠血症发生率22.41%,高钠血症为5.17%。发生钠代谢失衡的患者意识障碍发生率、脑血管痉挛发生率、病死率均高于正常血钠组,低钠血症发生脑血管痉挛的危险较其他2组高。结论蛛网膜下腔出血患者发生钠代谢失衡与疾病本身的病理生理机制有关。低钠血症的发生率高于高钠血症,高钠血症一旦发生很难纠正,应积极消除造成高钠血症的因素,以预防为主。低钠血症与脑血管痉挛相关,发生后要及时纠正,要注意补钠的方法与速度。     

196例原发性蛛网膜下腔出血并发症临床分析

目的通过分析原发性蛛剧膜下腔出血并发症的机制、临床特点及治疗，提高对蛛网膜下腔出血并发症的诊治水平。方法回顾分析196例蛛网膜下腔出血并发症的机制、特点及治疗情况。结果196例蛛网膜下腔出血患者再出血26例，发生率13．27％，脑血管痉挛33例，发生率16．84％，脑积水8例，发生率4．08％，脑梗死14例，发生率7．14％，低钠血症17例，发生率8．67％。结论早期发现和及时治疗各种并发症，对蛛网膜下腔出血预后至关重要。     

蛛网膜下腔出血合并低钠血症的临床研究

目的 探讨蛛网膜下腔出血(SAH)合并低钠血症的发生率、临床特点及发生机制.方法 分析69例SAH患者的临床、血清钠及DSA资料.结果 本组低钠血症发生率为69.6%,低钠血症开始发生时间为(5.6±3.8)天,低钠血症发生最严重的时间为(8.6±3.5)天.SAH并发低钠血症者发生脑血管痉挛(CVS)的发生率高于不伴低钠血症的SAH患者(P＜0.05),前交通动脉瘤破裂所致的SAH患者更易发生低钠血症(P＜0.001),治疗方法选择与发生低钠血症无明确关系(P＞0.05).结论 临床应对SAH患者并发低钠血症予以重视.     

动脉瘤性蛛网膜下腔出血后脑血管痉挛危险因素的分析

目的 探讨动脉瘤性蛛网膜下腔出血后脑血管痉挛的危险因素.方法 回顾性分析93例动脉瘤性蛛网膜下腔出血患者的临床资料,研究脑血管痉挛的危险因素.结果 93例动脉瘤性蛛网膜下腔出血患者中共有28例患者(30.1％)发生脑血管痉挛.Hunt-Hess分级≥Ⅲ级血管痉挛发生率明显高于Hunt-Hess分级Ⅰ-Ⅱ级,差异有统计学意义(P＜0.01);Fisher分级≥Ⅲ级血管痉挛发生率明显高于Fisher分级Ⅰ-Ⅱ级,差异有统计学意义(P＜0.01);白细胞计数＞ 15×109的患者脑血管痉挛发生率(41.9％,18/43)明显升高(P＜0.05).结论 Hunt-Hess分级≥Ⅲ级、Fisher分级≥Ⅲ级、白细胞计数增高是蛛网膜下腔出血后脑血管痉挛的危险因素.     

蛛网膜下腔出血后脑血管痉挛及再出血临床分析

目的通过分析蛛网膜下腔出血后脑血管痉挛及再出血的临床诊治、总结经验以提高对这两个合并症的诊治水平。方法对１２５例蛛网膜下腔出血患者的临床表现,诊治情况进行总结分析。结果１２５例蛛网膜下腔出血中３０例出现脑血管痉挛,占总数的２４％,其中２例死亡。应用钙拮抗剂组脑血管痉挛发生率明显低于未应用钙拮抗剂组,两组相比有显著性差异,再出血２２例,占总数１７．６％,１２例死亡。此两种并发症占总死亡率的８２．４％。结论早期应用钙拮抗剂可预防或降低脑血管痉挛发生率,从而减少蛛网膜下腔出血严重并发症。再出血是蛛网膜下腔出血死亡的主要原因之一。     

西比灵预防蛛网膜下腔出血后脑血管痉挛的疗效观察

目的：观察西比灵预防蛛网膜下腔出血后脑血管痉挛的疗效。方法：84例发病24h内入院的蛛网膜下腔出血患者随机分为治疗组和对照组。治疗组予西比灵5mg，口服2/d，同时予止血、镇静、止痛、脱水等常规治疗。对照组予尼莫地平60mg口服，4/d，止血、镇静、止痛、脱水等治疗同治疗组。结果：治疗组4例出现脑血管痉挛，占9．5％；对照组3例出现脑血管痉挛，占7．1％。两组脑血管痉挛发生率无显著差异（P＞0．05）。结论：口服西比灵预防蛛网膜下腔出血后脑血管痉挛有效。     

蛛网膜下腔出血后脑血管痉挛与脑脊液免疫球蛋白的关系

检测４１例蛛网膜下腔出血病人脑脊液中免疫球蛋白Ｇ的含量，其中２２例为蛛网膜下腔出血后伴脑血管痉挛患者，其脑脊液中免疫球蛋白Ｇ含量为８３．０４±３１．７８ｍｇ／Ｌ，１９例不伴脑血管痉挛病人，脑脊液中免疫球蛋白Ｇ含最为：３０．７９±２２．１３ｍｇ／Ｌ；脑血管痉挛组脑脊液中免疫球蛋白Ｇ含量明显高于非脑血管痉挛组（Ｐ＜０．０１）。结果表明蛛网膜下腔出血后脑血管痉挛有免疫反应的存在。     

原发性蛛网膜下腔出血合并低钠血症临床与预后分析

目的探讨原发性蛛网膜下腔出血（SAH）急性期低钠血症（HN）的原因、发生情况、干预方法及其对预后的影响。方法首次发病的急性期SAH病人190例，测定血清钠，对发生HN患者分析其病因并给予不同的处理。结果SAH后HN占同期原发性SAH的45．3％；并发HN者死亡率、脑血管痉挛（CVS）和继发性脑梗死、脑积水的发生率均显著高于血钠正常者（P〈0．05）；本组总死亡率为17．8％，低于文献报道。结论SAH后HN发生率很高；是预后差的危险因素；且与CVS、脑积水关系密切；其原因为脑性盐耗竭综合征和抗利尿激素分泌失调综合征，应针对病因治疗。     

他汀类药物预防蛛网膜下腔出血患者迟发性脑血管痉挛疗效的荟萃分析

目的 评价他汀类药物对蛛网膜下腔出血患者迟发性脑血管痉挛的预防作用。方法通过关键词“Statin”和“Subarachnoid hemorrhage”及对应的中文关键词“他汀”和“蛛网膜下腔出血”分别搜索Pubmed数据库、EMBASE数据库、0VID循证数据库、中国期刊网等中英文数据库，寻找研究指标包括迟发性脑血管痉挛的研究，应用Review Manager 4．2软件进行分析。结果 共获取符合要求的文献5篇，含2篇中文文献；3项研究采用了安慰剂对照；使用他汀类药物对于蛛网膜下腔出血患者发生迟发性脑血管痉挛的比值比（OR）为0．34，95％CI；0．20—0．60，P=0．0002；有统计学意义。他汀类药物对于蛛网膜下腔出血患者死亡的0R值为0．67，95％CI；0．33—1．39，P=0．29，无统计学意义。结论 目前文献支持他汀类药物可有效预防蛛网膜下腔出血患者发生迟发性脑血管痉挛，且对病死率无明显影响。     

中枢性低钠血症与非创伤性脑出血的相关研究

目的研究中枢性低钠血症与非创伤性脑出血患者的预后及出血部位的关系。方法分析397例脑出血患者,分为低钠血症及正常血钠两组,研究其死亡率差异以及低钠血症与出血部位的关系。结论 397例患者中58例患者发生低钠血症,1例诊断抗利尿激素分泌异常综合征(SIADH),57例为脑耗盐综合征(CSWS),死亡10例,采用χ2检验,低钠血症死亡率高于正常血钠组(P=0.014,P<0.05),低钠血症与死亡率呈正相关(Pearson相关系数r=0.123);两组脑出血部位分布不同,低钠血症患者中蛛网膜下腔出血多于基底节区出血,频数差异有显著性(P=0.01,P<0.0125)。结果中枢性低钠血症发生与脑出血部位相关,中枢性低钠血症中CSWS较SIADH更易发生。低钠组患者死亡率明显增高,血钠水平可预测疾病危险程度。     

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.