急性重型脑损伤患者脑组织氧代谢监测及意义

目的　探讨对急性重型脑损伤患者行脑组织氧代谢监测的临床意义。　方法对2 8例急性重型脑损伤患者 (均在全麻下急诊行血肿清除术和 (或 )去骨瓣减压术 )术中及术后持续进行脑组织氧代谢监测 ,观察脑组织氧分压 (PbtO2 )、二氧化碳分压 (PbtCO2 )和pH值 (pHbt)的变化。　结果　 (1) 2 8例脑外伤患者在剪开硬脑膜后PbtO2 、pHbt分别从 (13± 4 )mmHg、(6 .96± 0 .15 )增加至 (2 1± 5 )mmHg、7.0 5± 0 .12 (P <0 .0 5 ) ,PbtCO2 从 (6 1± 6 )mmHg下降至 (5 3± 5 )mmHg(P <0 .0 5 )。(2 )其中 2 4例脑外伤患者在血肿清除后 ,PbtO2 、pHbt值分别从 (2 1± 4 )mmHg、7.0 5± 0 .11增加至 (2 8± 6 )mmHg、7.15± 0 .10 (P <0 .0 5 ) ,PbtCO2 从 (5 2± 6 )mmHg下降至 (4 5± 4 )mmHg(P <0 .0 5 )。 (3)PbtO2 <10mmHg持续 30min以上的患者预后差。　结论　 (1)脑组织氧代谢监测是一种安全、可靠的监测手段 ,能直接动态反映脑组织的病理生理变化 ,及时发现脑组织缺血缺氧 ,以指导治疗。 (2 )持续进行脑组织氧代谢监测可判断重型脑外伤患者的预后。     

N-乙酰半胱氨酸对脑死亡巴马小型猪心脏的保护作用及其机制

目的 探讨N-乙酰半胱氨酸（NAC）对脑死亡状态下巴马小型猪心脏形态与功能的影响。方法 应用改进的缓慢间断颅内加压法建立巴马小型猪脑死亡模型。将实验动物随机分为3组，每组5只。对照组（A组）：动物麻醉后仅行开颅与开关腹手术。非药物干预组（B组）：建立脑死亡模型，不进行药物干预。NAC处理组（N组）：建立脑死亡模型，于脑死亡后1和12h，按200mg／kg的剂量将NAC加入100ml生理盐水中，经静脉缓慢滴注。分别于脑死亡后6、12和24h检测各组血清中肌钙蛋白T（cTnT）的水平以及干扰素α（TNF-α）、白细胞介素1β（IL-1β）以及白细胞介素6（IL-6）含量。脑死亡后24h，取各组心尖部心肌组织，光镜下观察心脏组织结构变化，电镜下观察心脏组织超微结构变化，免疫组织化学染色法观察核因子κB（NF-κB）的表达水平，逆转录聚合酶链反应（RT-PCR）检测NF-κB mRNA的变化。结果 脑死亡6h后，B组及N组的血清cTnT、IL-1β、IL-6、TNF-α水平均开始升高，但N组升高幅度显著低于B组。脑死亡后24h可见心肌细胞出现损伤性改变；N组心肌细胞损伤明显轻于B组。B组及N组心肌细胞中NF-κB mRNA及其蛋白表达水平均升高，但N组显著低于B组。结论 N-乙酰半胱氨酸能够减轻脑死亡状态下心脏的形态和功能损伤性改变，其机制可能与抑制NF-κB mRNA及其蛋白的表达，减少炎症介质的释放有关。     

带状灰质异位的磁共振弥散张量白质束成像研究

目的采用磁共振弥散张量白质束成像技术,观察带状灰质异位脑白质异常分布情况,探讨异位灰质的神经病理机制以及弥散张量白质束成像技术的应用价值。方法采用磁共振弥散张量白质束成像技术,对1例癫痫症状的带状灰质异位患者进行白质束描绘,观察其不同灰、白质的分布情况,并和1例正常人进行对比研究。结果弥散张量白质束成像技术很好地描绘了白质束结构。整体观察发现带状灰质异位患者脑白质整体结构紊乱,与正常人相比其联络弓状纤维稀疏、大部缺失,胼胝体纤维稀疏不整;局部分析发现内层灰质为主要的白质纤维发出处,而外层灰质仅发出细碎短小的纤维。结论对于带状灰质异位,异位的内层灰质不仅具有神经生理功能,并且可能起着主要作用,外层"正常"的灰质由于脑结构紊乱而丧失主要功能地位;灰质结构的紊乱导致白质纤维结构的缺失;弥散张量白质束成像技术可以很好地应用于带状灰质异位的神经机制研究。     

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     

Cerebral venous malformation complicated by spontaneous thrombosis

A case of spontaneous thrombosis and infarction leading to death as complications of a cerebral venous malformation in a 13-yearold boy is reported. This is the first published report of this type of complication occurring in a case of venous angioma. While the biologic behavior of cerebral venous malformations has suggested that they are benign in nature, and the results of surgical management have encouraged a conservative approach, the present case illustrates a potential complication and argues against the assumption that these malformations are completely benign in nature.     

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.