青年自发性脑出血的病因及诊治

目的 探讨青年人自发性脑出血的病因及诊断治疗特点。方法分析42例自发性脑出血青年患者(年龄在45岁以下)的临床资料，其均急诊行CT检查，根据病情采取不同的治疗方法，其中手术治疗24例，血管内介入治疗5例，保守治疗13例。结果病因中AVM最常见．其次高血压，部分病因未明。AVM引起的青年自发性脑出血有82．4％(14／17)位于脑叶，高血压性脑出血有66．7％(8／12)位于脑基底节，75％(9／12)的高血压性脑出血患者年龄在40-45岁之间。治愈27例，好转12例，死亡3例。结论青年自发性脑出血最常见的病因是。AVM，AVM所致的脑出血主要位于脑叶。高血压性脑出血主要位于脑基底节，其发病率与年龄有明显的相关性。只要诊断及时，治疗得当．青年自发性脑出血一般预后良好。     

脑出血继发脑梗死30例的CT与临床

目的探讨脑出血继发脑梗死的临床特点。方法分析30例脑出血继发脑梗死的CT及临床资料。结果脑出血继发脑梗死多为腔隙性梗死，发生梗死后多无症状，给予活血化瘀或量子血疗治疗病情好转，无加重。结论脑出血继发的脑梗死主要依靠CT诊断，确诊后要及时治疗，不必等到血肿完全吸收后再按脑梗死治疗。     

儿童自发性脑出血的病因及诊治

目的探讨儿童自发性脑出血的病因及其诊治，方法对30例自发性脑出血儿童患者的临床资料进行回顾性分析。30例患者中保守治疗5例，手术治疗13例，血管内栓塞后再手术治疗4例，γ-刀治疗3例。结果本组30例中有15例脑动静脉畸形引起，30例中治愈23例，好转5例，死亡2例。随访23例，22例健康生存，1例再出血死亡。结论脑动静脉畸形是儿童自发性脑出血最常见原因，及时诊断治疗，预后良好。     

微创手术治疗高血压脑出血

目的 探讨微创手术治疗高血压脑出血的有效性和治疗原则。方法 总结分析微创于术治疗62例高血压脑出血的临床资料。结果 恢复良好6例，有功能障碍但生活能自理22例，清醒但生活不能自理31例，死亡3例。结论 超早期及早期微创开颅术清除血肿是高血压脑出血较好的救治方法，病例的选择、手术技巧及术后处理直接影响治疗效果。     

无头痛症状脑出血20例

目的无头痛症状脑出血是脑出血患者的不典型表现，易延误诊治，应提高警惕。方法取本院187例脑出血中20例无头痛症状的临床资料。结果20例无头痛症状脑出血经治疗好转7例，治愈13例，无死亡，预后较好。结论无头痛症状脑出血应根据其临床表现及时行CT检查，并进行适宜治疗，以减少致残致死率。     

路路通过脑出血治疗的动物实验及临床观察

目的 探讨路路通治疗脑出血的实验评价及临床疗效。方法 采用兔脑出血模型及住院脑出血患者静脉注射路路通,利用病理及影像学评价疗效。结果 动物实验及临床观察均显示对照组和治疗组差异显著。结论 路路通对于脑出血急性期有显著疗效。     

妊高征性脑出血手术治疗13例临床分析

妊高征性脑出血临床少见，其起病急，发病迅速，抢救不及时使产妇致残，甚至死亡。我院自1991年12月至2002年12月，共对13例妊高征性脑出血进行手术治疗，取得了很好的临床效果。     

急性脑出血治疗中尼膜同的应用研究

目的 观察尼膜同治疗急性脑出血的临床疗效。方法 应用前瞻性随机单盲方法，对１８２例经ＣＴ证实的急性脑出血病人，在起病７２小时内随机分为尼膜同和甘露醇组（尼膜同组）及单纯甘露醇组（对照组），采用神经功能缺损程度积分差及ＣＴ上血肿吸收率为指标，比较两组疗效。结果 尼膜同组在各个时点上神经功能缺损的平均减少分数以及ＣＴ上血肿吸收率均优于对照组。结论 尼膜同是治疗急性脑出血的一种安全、有效的药物。     

射流冲洗治疗高血压脑出血临床研究

高血压脑出血是神经科急危重症，死亡率及致残率高，自11年（CU8hing）首先使用手术方法治疗后，在半个多世纪内有了许多改进，但效果仍不佳。80年代后，随着CT广泛应用，脑出血诊断及精确定位都已解决，临床上广泛开展了锥颅抽吸术及碎吸术，因其易造成再出血，清除血肿盲区大而影响了治疗效果。我们采用YLI．10型颅内血肿粉碎穿刺针治疗高血压脑出血ito例［’」，证明本法具有清除完全，安全易行，速度快，不易造成再出血，损伤小的优点。报告如下：1资料和方法1．1＃具YLI－10型颅内血肿穿制粉碎由穿刺针。血肿粉碎器及充电式手电钻…     

中重症高血压脑出血的外科治疗（附36例临床分析）

中重症高血压脑出血的外科治疗（附３６例临床分析）金国良，阎晓勤高血压脑出血是一种预后严重的疾病，对中、重症患者需行外科治疗的观点近来也已基本确立。现将我院１９９１年１月～１９９４年１２月间经手术治疗的３６例中、重症患者，结合有关文献进行分析。临床资料...     

Genetic findings in obsessive-compulsive disorder in childhood and adolescence and in adulthood

Obsessive-compulsive disorders (OCD) are on the rise, and affected children, 1-2% of the general population, often are seriously impaired in their development. OCD is characterized by recurrent, intrusive and disturbing thoughts as well as by repetitive stereotypic behaviours. Depending on their age and developmental status, patients usually try unsuccessfully to suppress the obsessive thoughts and compulsive behaviours. The current state of genetic research on OCD and early-onset OCD is presented and discussed. OCD, especially early-onset OCD, has been shown to be familial. Convincing evidence indicates that both environmental and genetic factors substantially influence OCD. Various approaches, including linkage and association studies, yielded conflicting results as well as the notion that multiple genes of modest effect sizes, in interaction with environmental factors, cause vulnerability to the disorder. The phenotypic and genetic heterogeneity of OCD complicate the identification of specific genetic factors. Further studies have to be designed in consideration of subtypes, e.g. age at onset, symptom dimensions, or comorbid disorders.     

Changes in extra- and intracellular pH in the brain during and following ischemia in hyperglycemic and in moderately hypoglycemic rats

Incomplete forebrain ischemia of 15-min duration was induced in rats made hyperglycemic or moderately hypoglycemic prior to ischemia. Tissue CO2 tension, CO2 content, labile tissue metabolites, and extracellular pH (pHe) were measured, and intracellular pH (pHi) was derived by calculation on the assumption that cerebral intracellular fluids can be lumped into one space. In hypoglycemic animals, mean tissue lactate content increased from 2 to 10 mumol g-1. Tissue CO2 content was virtually unchanged and the CO2 tension increased from approximately 50 to approximately 145 mm Hg. In hyperglycemic animals, tissue lactate content rose to 20 mumol g-1, and the CO2 content decreased by 25%, demonstrating that some CO2 was lost to the blood supplied by the remaining perfusion. Accordingly, tissue CO2 tension did not rise above 200 mm Hg. pHe was reduced in proportion to the amount of lactate accumulated, the values obtained in hypo- and hyperglycemic animals showing relatively little scatter (6.76 +/- 0.03 and 6.25 +/- 0.04, respectively). In hypoglycemic animals the extracellular HCO-3 concentration was virtually unchanged, demonstrating that any influx of lactic acid from the cells must have been accompanied by H+ efflux and/or HCO-3 influx via independent routes. In hyperglycemic animals [HCO-3]e fell by greater than 10 mumol ml-1. In both groups [HCO-3]e was reduced during the first 5 min of recovery. Recovery of pHe was slower in hyper- than in hypoglycemic animals. During ischemia calculated pHi fell to 6.37 +/- 0.04 and 5.95 +/- 0.06 in hypo- and hyperglycemic animals, respectively. Differences in pHi were maintained for the first 15 min of recovery, but in both hypo- and hyperglycemic animals pHi had normalized after 30 min. It is concluded that preischemic hyperglycemia leads to a more pronounced intra- and extracellular acidosis than normo- and hypoglycemia, an acidosis that also resolves more slowly during recirculation.     

Dopamine-derived alkaloids in alcoholism and in Parkinson's and Huntington's diseases

Summary Tetrahydroisoquinoline (TIQ) alkaloids and 1-carboxy TIQ derivatives have been found in human fluids and/or tissues. The possible biosynthetic pathways of salsolinol (Sal), taken as an example of TIQs, are discussed, and the possibility that biosynthesis occurs through a stereospecific enzymatic reaction is considered. In this respect, it is reported that the R enantiomer of Sal predominates in urines of healthy volunteers, whereas the S enantiomer predominates in port wine and possibly in other beverages and foods, suggesting that Sal present in humans could have, at least partially, and endogenous enzymatic origin.TIQs and other dopamine-derived alkaloids are weak MAO inhibitors, the R enantiomer of Sal and salsolidine being more potent than the S form.The changes in monoamine oxidase activity and the nigrostriatal concentrations of dopamine and homovanillic acid in Parkinson's and Huntington's diseases and in alcoholism are reviewed. In these pathological situations, changes in the levels of dopamine-derived alkaloid levels may occur. The possibility that the modifications found might cause or contribute to changes in mental and/or neurophysiological states in these pathological situations is considered.