外伤性嵌钝性天幕疝的发生及天幕切开疗效的初探

目的 :为了解外伤性嵌钝性脑疝的发生规律 ,认识天幕切开治疗嵌钝性脑疝的疗效 ,对术前确诊为脑疝的病例术中清除血肿后直接观察脑疝的嵌钝情况。方法 :对脑疝嵌钝者行天幕切开 ,观察其术后 GCS评分同时与既往临床资料上分析嵌钝性脑疝可能性较大、未切开天幕的病例进行对比。结果 :嵌钝性脑疝多发生在血肿量大 ,GCS评分低的病人。结论 :天幕切开可提高疗效。     

中药配合低能量氦—氖激光血管内照射为主治疗缺血性中风疗效观察

目的：观察中药配合低能量氦－氖激光血管内照射为主治疗缺血性中风疗效。方法：治疗组：用中药配合低量氦－氖激光血管内照射为主治疗缺血性中风６９例;对照组：用降纤酶、尼莫通治疗缺血性中风４２ 例。结果：治疗组基本痊愈４８ 例,显效８例,有效７例,无效５ 例,恶化１ 例,有效率为９１．３０％ 。对照组基本痊愈２０例,显效１例,有效９ 例,无效１１ 例,恶化１例,有效率为７１．４３％ 。经χ２ 检验,χ２＝ ７．６,Ρ＜ ０．０１,有显著差异。结论：治疗组中药配合低能量氦－氖激光血管内照射为主治疗缺血性中风综合疗效明显优于对照组用降纤酶和尼莫通治疗缺血性中风     

大鼠局灶性脑缺血模型及其与C反应蛋白变化的关系

目的 改进大鼠大脑中动脉梗塞法,建立更接近于临床缺血性脑卒中及其再扩灌注的可靠模型,并观察其与血甭Ｃ反应蛋白变化的。方法沿大鼠右颈内动脉插入长２．１￣２．３ｃｍ直径０．２０５ｍｍ的单股尼龙丝,直达大脑中动脉起始部开口,阻断其血流,观察大鼠神经病学改变及脑组织形态学变化,并测定血清Ｃ反应蛋白含量。结果 术后大鼠表现特殊体态及典型追尾征,６ｈ大脑中动脉供血区出现缺血性外观（ＴＴＣ染色）及相应组织学变化     

Eating despite severe difficulties: assessment of poststroke eating

• ? A programme for the assessment and nursing diagnoses of eating difficulties among stroke patients was tested. The patients' experiences regarding eating were expressed in interviews and dialogues. Eating was observed during both a test meal and regular meals.
• ? The assessments included the prerequisites for eating as well as oral, pharyngeal and oesophageal functions.
• ? General and specific nursing diagnoses as well as life consequences (handicap) were established, based on assessment of disabilities and impairments, and interviewing the patients and their families, respectively. The general nursing diagnoses were formulated on admission after the test meal and these were reformulated to form specific nursing diagnoses after assessments of the functions.
• ? The programme presented proved to be useful in clinical practice. It is emphasized that many assessments must be co-ordinated for each individual.

     

Cell Type-specific Effects of the Neural Adhesion Molecules L1 and N-CAM on Diverse Second Messenger Systems

We have previously shown that the neural adhesion molecules L1 and N-CAM influence second messenger systems when triggered with specific antibodies at the surface of the phaeochromocytoma PC12 cell line (Schuch et al., Neuron, 3, 13 - 20, 1989). To determine whether the two molecules are linked to the same intracellular signalling cascades, independent of the cell type expressing them, or whether different neural cell types respond with different signal transduction mechanisms, we have investigated the effects of antibodies to L1 and N-CAM, and the isolated molecules themselves, on second messenger systems in different neural cell types. We have investigated cultures of cerebellar and dorsal root ganglion neurons and transformed Schwann cells and related these results to those obtained with the PC12 cell line. Here we show that addition of L1 and N-CAM antibodies and the isolated molecules themselves elicit cell type-specific responses that can be modulated by the substrate on which the cells are maintained. Depending on the cell type, cells respond to the triggering of L1 and N-CAM with antibodies, or addition of the purified molecules, by either up-regulation or down-regulation of inositol phosphate turnover, by a rise in intracellular Ca2+ levels dependent on or independent of the opening of voltage-gated Ca2+ channels, or by an increase or decrease in intracellular pH. Moreover, cerebellar neurons expressing N-CAM respond to addition N-CAM, but not to N-CAM antibodies, in contrast to the other neural cell types studied, which respond to both triggers. Furthermore, cerebellar neurons were the only cells to show a rise in cAMP levels in response to any of the ligands tested. This stimulation of cAMP production by L1 antibodies depended on the cross-linking of L1 molecules at the cell surface, whereas the other responses did not depend on clustering of L1. Simultaneous addition of L1 and N-CAM antibodies either elicited an additive or more than additive effect on the intracellular responses which, for cerebellar neurons, depends on the substrate on which the cells are maintained. These observations indicate that L1 and N-CAM or their antibodies activate cell type-specific intracellular signalling systems and that the two molecules can act interdependently or independently of each other.     

Perioperative stroke Part I: General surgery,carotid artery disease,and carotid endarterectomy

Although stroke, defined as a focal neurological deficit lasting more than 24 hr, is uncommon in the perioperative period, its associated mortality and long-term disability are high. No large-scale data are available to identify the importance of recognized risk factors for stroke in the perioperative period. A review of the literature shows that the incidence and mechanism of its occurrence are influenced by the presence of cardiovascular disease and the type of surgery. The most common cause of perioperative stroke is embolism. In non-cardiac surgery, the incidence of perioperative stroke is higher among the elderly. Properly administered, controlled hypotension is associated with minimal risk of stroke. Cerebral vasospasm may be the cause of focal cerebral ischaemia in eclamptic patients, and the aggressive treatment of hypertension may exacerbate the neurological damage. The risk of stroke associated with carotid endarterectomy is closely related to the preoperative neurological presentation, and the experience of the surgical/anaesthetic team. Symptomatic cerebrovascular disease, acute stroke, asymptomatic carotid lesions, preoperative assessment of risk, local and general anaesthesia, cerebral protection and monitoring during carotid endarterectomy are discussed with reference to reducing the risk of perioperative stroke. Adequate monitoring and protection have minimized the risk of ischaemia from carotid clamping, and the major mechanism of stroke is embolization.     

Impaired cerebral autoregulation 24 h after induction of transient unilateral focal ischaemia in the rat

Cerebral blood flow (CBF) and cerebral autoregulation have been investigated 24 h after transient focal ischaemia in the rat. Cerebral blood flow was measured autoradiographically before and during a moderate hypotensive challenge, to test autoregulatory responses, using two CBF tracers, (99m)Tc-d,l-hexamethylproyleneamine oxide and 14C-iodoantipyrine. Prior to induced hypotension, CBF was significantly reduced within areas of infarction; cortex (28 +/- 20 compared with 109 +/- 23 mL/100 g/min contralateral to ischaemic focus, P = 0.001) and caudate (57 +/- 31 compared with 141 +/- 32 mL/100 g/min contralaterally, P = 0.005). The hypotensive challenge (mean arterial pressure reduced to 60 mmHg by increasing halothane concentration) did not compromise grey matter autoregulation in the contralateral hemisphere; CBF data were not significantly different at normotension and during hypotension. However, in the ipsilateral hemisphere, a significant volume of cortex adjacent to the infarct, which exhibited normal flow at normotension, became oligaemic during the hypotensive challenge (e.g. frontal parietal cortex 109 +/- 15% to 65 +/- 15% of cerebellar flow, P < 0.01). This resulted in a 2.5-fold increase in the volume of cortex which fell below 50% cerebellar flow (39 +/- 34 to 97 +/- 46 mm3, P = 0.003). Moderate hypotension induced a significant reduction in CBF in both ipsilateral and contralateral subcortical white matter (P < 0.01). In peri-infarct caudate tissue, CBF was not significantly affected by hypotension. In conclusion, a significant volume of histologically normal cortex within the middle cerebral artery territory was found to have essentially normal levels of CBF but impaired autoregulatory function at 24 h post-ischaemia.     

Blockade of the NMDA receptor increases developmental apoptotic elimination of granule neurons and activates caspases in the rat cerebellum

Elimination of neurons produced in excess naturally occurs during brain development through programmed cell death. Among the many survival factors affecting this process, a role for neurotransmitters acting on specific receptors has been suggested. We have performed an in vivo pharmacological blockade of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors, using the competitive NMDA receptor antagonist CGP 39551 at developmental stages corresponding to those at which a survival dependence on the stimulation of this receptor has been demonstrated for cerebellar granule neurons explanted in culture (typically from postnatal day 7 to postnatal day 11 or 13). We were able to demonstrate an increased level of DNA fragmentation in the cerebellum of the treated rats. At the P11 stage, in particular, the fragmented DNA extracted from the cerebellum of CGP 39551-treated pups showed a clear laddering of nucleosomal fragments after agarose-gel electrophoresis. Accordingly, in situ TUNEL technique showed a remarkable increase of cells positive for nucleosomal DNA fragmentation, particularly in the inner granular layer of the cerebellum of treated rats at P11 stage. Therefore, the natural rate of apoptotic elimination of cerebellar granule neurons is considerably enhanced under conditions of pharmacological blockade of the NMDA receptor, thus demonstrating, for the first time in vivo, a clear survival dependence of these neurons upon the stimulation of the NMDA receptor. Concomitantly with the increased rate of apoptotic elimination of granule neurons, the activity of two death proteases of the caspase family, in particular of caspase 3 and caspase 1 at a lower extent, was remarkably increased in the cerebellum of the treated rats. On the contrary, a marker related to the normal differentiation process of granule neurons, the enzyme ornithine decarboxylase, was strongly decreased in its activity in the cerebellum of treated rat pups.     

珍珠七十丸对SHRsp脑卒中及高血压防治作用的研究

目的 :研究珍珠七十丸对卒中型自发性高血压大鼠 (SHRsp)血压、体重、脑卒中及生存率的影响。 方法 :8周龄SHRsp按血压水平随机分为 3组 ,即对照组、珍珠七十丸预防组与治疗组 ,每组 10只 ,其中预防组于分组后灌胃给予珍珠七十丸每天 150mg·kg^-1,治疗组于 10周龄开始灌胃给予相同剂量。实验期间每天观察动物饮食、行为活动及存活情况 ,每周称体重 ,每2周测定血压 ,记录SHRsp脑卒中首次发作时间。结果 :珍珠七十丸对遗传性高血压有良好的防治作用 ,治疗组及预防组血压均较同期对照组血压低 (P<0.05或P<0.01)。珍珠七十丸可改善SHRsp动物一般行为活动 ,预防组动物体重持续增加 (P<0.05或P<0.01) ;治疗组动物体重在 14周龄时亦明显大于同期对照组 (P<0 .05)。对照组有 60%动物发生脑卒中 ,其中 20%死亡 ,而预防组及治疗组仅各有 20%动物发生脑卒中 ,且没有动物死亡。结论 :珍珠七十丸具有明显的降压作用 ,对高血压引起的脑卒中也有一定的保护作用。     

药物性生理失调的后果-畅销镇痛药罗非昔布另解

Selective cyclo-oxygenase-2(COX-2) inhibitor, VI-OXX(rofecoxib), was voluntarily withdrawn worldwide from drugstores by its maker Merck & Co., Inc. on Sep-tember 30, 2004, for its potential lethal side effects of heart attack or stroke.