外伤性股动脉栓塞继发肾功能衰竭32例的综合治疗

目的 探讨外伤性股动脉栓塞后继发急性肾功能衰竭的临床综合治疗。方法 对32例外伤性股动脉栓塞术后继发急性肾功能衰竭病例均进行急诊手术切开取栓、血管吻合术，术后均予以综合治疗。结果住院时间7天-3个月，平均41d。最终截肢6例，死亡2例，24例修复成功。结论 术前准确判断预后，正确选择手术方式、术中筋膜减张性切开、术后及时清除坏死组织、术后利尿合剂应用和及时必要的血透是影响外伤性股动脉栓塞保肢术后急性肾功能衰竭预后的重要因素。     

早期扩髓髓内钉固定治疗合并胸部损伤的股骨干骨折

目的探讨合并胸部损伤的股骨干骨折早期扩髓及髓内钉固定是否增加并发症及死亡率. 方法采用回顾性对比分析,依据下列标准选择病例(1) 年龄在17～65岁;(2) 必须有胸部损伤[简明损伤定级(AIS)≥2], 且损伤严重度评分(ISS)≥16;(3) 住院时间≥48 h;(4) 病史中无明显影响全身状况的疾病, 如糖尿病, 慢性心、肺、肾功能不全等;(5) 有股骨干骨折, 且进行了扩髓髓内钉固定, 不含钢板、外固定支架或牵引及石膏固定者.并按受伤至手术时间划分为两组, A组为<24 h手术者(早期扩髓组), B组为≥24 h手术者(延期扩髓组),将两组间合并伤情况、ISS、住院时间、ICU时间、并发症、死亡及合并休克情况进行比较. 结果有96例符合上述标准, 其中A组57例, B组39例,经统计学处理, 两组间仅在股骨开放性骨折发生率(A组53%,B组31%,χ2=4.496, P<0.05)、合并休克率(A组51%, B组28%,χ2=4.895, P<0.05 )及住院时间[A组为(17.5±6.5)d, B组为(31.5±9.5)d,t=8.599, P<0.001]上差异有显著性意义和非常显著性意义, 而两组并发症发生率和死亡率等方面比较, 差异无显著性意义(P>0.05). 结论在合并胸部损伤的股骨干骨折中,只要能控制休克,保证生命体征平稳,对股骨干骨折行早期扩髓髓内钉固定不增加患者的并发症发生率及死亡率,并可促进患者早日康复,缩短住院时间.     

颅内脑池显微解剖研究

目的通过对国人脑池显微解剖的研究,以指导显微神经外科手术和进一步理解影像学解剖的重要临床意义和应用价值。方法对15具经福尔马林固定的国人成年头颅标本的颅内各个脑池进行显微解剖研究,测量和描述各脑池的位置、大小、形态及结构。结果颅内重要的脑池有(1)嗅池:长度为(32.68±2.97)mm,宽度为(7.18±1.82)mm,深度为(7.20±1.27)mm;(2)视交叉池:侧壁长度为(14.88±3.07)mm,上表面前壁长(14.20±1.47)mm,后壁长(10.37±1.59)mm;(3)颈内动脉池:长度为(15.06±3.07)mm,宽度为(12.01±1.32)mm;(4)终板池:底边左侧长度为(8.99±1.15)mm,右侧长度为(21.00±1.09)mm,最大宽径为(16.42±2.58)mm;(5)脚间池:最大深度为(19.47±2.28)mm,池顶宽度为(11.35±2.85)mm;(6)脚池:为三角形,三边长度分别为(10.48±2.56)mm,(9.64±1.78)mm,(3.58±0.25)mm;(7)外侧裂池:上部长度为(18.63±2.02)mm,基底部长度为(38.08±3.22)mm,宽度为(5.65±0.92)mm,深度为(7.02±2.28)mm;(8)胼胝体池:平均最大宽径为(3.44±0.40)mm;(9)四叠体池:最大长径为(19.37±3.38)mm,最大宽径为(15.24±2.37)mm,最大前后径为(3.65±0.57)mm;(10)环池:为环形,最大宽度为(3.16±0.37)mm;(11)小脑延髓池:最大长度为(18.77±1.77)mm,最大宽度为(32.4     

Myxopapillary ependymoma of lumbosacral region with metastasis to both cerebellopontine angles: report of a rare case

Introduction Myxopapillary ependymomas are low grade tumours that are known to recur locally even after complete excision, but metastasis to distant sites is extremely uncommon. Case report We report an unusual case of lumbo-sacral myxopapillary ependymoma in a 13-year-old boy with metastasis to both cerebellopontine angles. To the best of our knowledge, this is the youngest patient of metastatic myxopapillary ependymoma.     

立体定向开放显微手术治疗脑内致痫小病灶

目的脑内致癫痫小病灶术前、术中的精确定位和病灶切除,是手术治疗效果的关键。探讨立体定向开放微创手术,皮层电极监测下切除脑内致痫小病灶的手术方法。方法53例症状性癫痫病例,CT、MR I检查有脑内小病灶(直径在0.5~3.0 cm),24 h视频脑电图确认致痫灶为脑内单发病灶。ASA 601S型立体定向仪CT引导辅助全麻环钻开颅,导针穿刺放置导管引导,显微镜下手术分离、切除病灶,皮层脑电图确认将致痫灶切除。结果病灶全切率达96.2%,术后50例得到随访,随访时间5~12个月,平均6.3个月,癫痫消失45例,脑电图检查记录到癫痫波11例,临床癫痫发作5例。因肺癌死亡3例。结论CT立体定向引导,显微手术切除颅内致痫小病灶,术中皮层电极确认将致痫灶切除,是一种定位精确、微创、安全、有效的治疗方法。     

Disseminated intracerebral alveolar echinococcosis: CT and MRI

Cerebral alveolar echinococcosis is rare and has a poor prognosis. We report an unusual case presenting with disseminated intracranial lesions secondary to primary hepatic infection. Received: 2 May 1996 Accepted: 23 August 1996     

兔局灶脑缺血后脑片[Ca~(2 )]i的变化

目的：研究脑缺血后脑片[Ca2＋]i变化。方法：采用新型Ca2＋荧光指示剂Fura－2双波长法测定兔大脑中动脉阻塞（MCAo）局灶脑缺血后脑片细胞内游离钙（[Ca2＋]i）。结果：脑缺血后脑组织[Ca2＋]i显著升高。结论：[Ca2＋]i在脑缺血损害中起重要作用。     

Malignant evolution of presumed benign lesions in the brain in neurofibromatosis: case report

We report a patient suffering from neurofibromatosis type 1 in whom neoplasms developed from the areas of altered signal which are generally considered benign and typical of the disease. MRI, despite two previous examinations 3 and 2 years before development of the tumour, gave no clue to an unfavourable outcome. Received: 18 January 1996 Accepted: 24 October 1996     

Chronic parasite infection in mice induces brain granulomas and differentially alters brain nerve growth factor levels and thermal responses in paws

Schistosoma mansoni infection, both in humans and in animal models, is known to induce granulomas in the liver and intestine. It has also been reported that in humans the eggs of this parasite can reach the brain, causing psychiatric and neuropathological disorders. Whether this also occurs in rodents is unknown. To answer this question, mice were infected with this parasite and the central nervous system (CNS) examined at various time intervals. The results show that schistosomiasis induced granulomas in several regions of the CNS and increased nerve growth factor (NGF) levels in the cortex, hypothalamus and brain stem, but not in the hippocampus. The infection also caused paw hyperalgesia, as determined by the hot-plate test, and a local increase in NGF, but not in substance P. These findings indicate that the murine model of infection can be used for studying mechanisms leading to human neuroschistosomiasis and suggest that the neuropathological disorders and the sensory deficits observed in human schistosomiasis are associated with impaired levels of NGF in the peripheral and central nervous system. Received: 18 January 1996 / Revised, accepted: 16 April 1996     

Acute cerebral infarction: pathophysiology and modern treatment concepts

Summary This review focuses on the pathophysiological changes in acute cerebral ischemia, with special emphasis on disturbances of the cerebral blood flow (CBF) and the associated penumbra concept. Alternatively, the model of peri-infarct depolarization is demonstrated. Metabolic and molecular changes caused by cerebral ischemia and reperfusion are discussed, namely energy failure, release of glutamate with an excitatoric burst, calcium influx in neurons, generation of free radicals, activation of different proteases, disturbances of protein synthesis, induction of gene expression and apoptosis, loss of membrane integrity, edema formation and microvascular disturbances. In summary, the pathophysiological changes after focal cerebral ischemia and reperfusion are most adequately described by a network of interacting different mechanisms of tissue alterations. The simple concept of a cascade of ischemic effects which would be easy to block seems to be less applicable. A time window of approximately 6 h for the acute stroke therapy is postulated on the base of the above mentioned pathophysiological changes. The recently introduced treatment regimen with optimized basic treatment, recanalization using thrombolysis and neuroprotection by different agents is presented. Different modes of a possible intervention are discussed. Modern concepts of stroke therapy including stroke-unit care and thrombolysis with add-on neuroprotection seem to have potential for improving the outcome of acute stroke patients.