大面积脑梗死20例外科治疗分析

目的 分析外科治疗大面积脑梗死的临床疗效.方法 20例急性大面积脑梗死患者均采用外科手术治疗,包括去大骨瓣减压、硬膜充分敞开、颞叶前部切除和梗死组织切除术,颞肌贴敷术等.结果 经术后1 a随访,存活15例,7例可生活自理,7例可部分生活自理,1例植物生存状态,死亡5例.结论 大骨瓣减压、颞叶前部切除并颞肌贴敷术是治疗急性大面积脑梗死的一种有效手段,可降低病死率、改善预后及生存质量.     

重型颅脑损伤术后大面积脑梗死的临床分析

目的 探讨重型颅脑损伤开颅术后大面积脑梗死的诊断与治疗.方法 总结本科2001年5月～2006年5月收治的12例重型颅脑损伤开颅术后大面积脑梗死的临床特点、CT或MRI诊断和治疗.结果 重型颅脑损伤开颅术后大面积脑梗死导致病情加重,出院时12例疗效评定中良好4例,中残3例,重残2例,植物生存1例,死亡2例.结论 重型颅脑损伤开颅术后病情发生变化时应及时复查CT或MRI,使其并发的大面积脑梗死及早得到诊断与治疗.     

重型颅脑损伤术后大面积脑梗死临床分析

目的 分析重型颅脑损伤开颅术后大面积脑梗死发生的相关因素及治疗效果. 方法 选择东莞市石碣医院神经外科自2002年1月至2008年4月收治的重型颅脑损伤行开颅术治疗的332例患者,其中术后出现大面积脑梗死20例,回顾性分析术后出现或未出现大面积脑梗死这两类患者术前GCS评分,出血量,颅底骨折,瞳孔变化,是否有脑疝存在及持续时间情况;采用标准大骨瓣减压术治疗及常规综合治疗,并对其疗效进行评价. 结果 术前GCS评分<5分、颅内出血量60 mL以上及颅底骨折合并脑疝持续时间长者大面积脑梗死发生率明显增加.本组20例患者随访12月.应用GOS评估预后,其中良好8例,中残3例,重残2例,植物生存3例,死亡4例.结论 开颅术后出现大面积脑梗死是多种因素所致,术前GCS评分越低、颅内出血量大、颅底骨折合并脑疝持续时间长是其发生的重要原因;及时发现并行标准大骨瓣减压、脱水降颅内压、改善脑循环、预防脑血管痉挛、亚低温等治疗可有效降低其致残率和病死率.改善预后.     

20例大面积脑梗死临床分析

目的 探讨大面积脑梗死的临床特点、预后,分析其危险因素,提出合适的治疗方案.方法 对20例大面积脑梗死患者的临床资料进行回顾性分析,总结其临床特点,危险因素,提出合适的治疗方案.结果 20例大面积脑梗死患者,意识障碍16例,头痛9例,呕吐12例,凝视11例,脑膜刺激征1例,继发出血3例,18例感染,死亡7例.房颤、糖尿病为其重要的危险因素.结论 大面积脑梗死进展快,意识障碍、头痛、失语、凝视多见,预后差,需及早使用脱水剂,尽早外科治疗,以降低病死率.     

大面积脑梗死的外科治疗

目的评价大面积脑梗死的外科治疗方法及效果。方法回顾性研究63例大面积脑梗死病例外科救治方法及效果。结果恢复良好39例(61.9%),中残8例(12.7%),重残9例(14.2%),植物生存2例(3.2%),死亡5例(12.0%)。结论经大骨瓣开颅加颞肌贴敷和术后给综合治疗,可使大面积脑梗死病死率明显下降,值得临床推广。     

东菱精纯克栓酶与依达拉奉联用治疗大面积脑梗死36例观察

目的 观察精纯东菱克栓酶联合依达拉奉治疗大面积脑梗死的疗效.方法 对36例大面积脑梗死患者给予精纯东菱克栓酶联合依达拉奉治疗.结论 精纯东菱克栓酶联合依达拉奉治疗大面积脑梗死能明显提高疗效,改善神经功能、是治疗大面积脑梗死的有效措施之一.     

去骨瓣减压术治疗大面积脑梗死(附30例报道)

目的 探讨去骨瓣减压治疗大面积脑梗死的意义、手术适应证及手术技巧。方法 回顾分析2010年7月～2015年7月江门市中心医院神经外科收治的30例大面积脑梗死行去骨瓣减压术患者的临床资料,总结分析其手术的意义、手术时机及手术操作的体会。结果 25例患者术后存活,5例死亡。去骨瓣减压术后格拉斯哥昏迷评分(GCS)较术前明显改善(t=-5.08,P<0.05)。术前瞳孔散大24例,术后有16例瞳孔缩小(80%)。术后绝大多数病例CT中线移位较术前回复(28/30)。术后3个月时GOS评分4分7例,3分17例,2分1例,1分5例。结论 去骨瓣减压术是大面积脑梗死的有效治疗手段,早期外科干预、术中充分减压可提高大面积脑梗死患者的生存率。     

颅脑外伤术后并发大面积脑梗死的临床特点及治疗分析

目的探讨颅脑外伤术后并发大面积脑梗死的发病原因、临床特点及治疗方法。方法总结13例CT证实为颅脑外伤术后大面积脑梗死病人的临床资料，复习相关文献。结果所有病例在发现大面积脑梗死后均采用综合治疗，并随访半年，按GOS标准判断预后，恢复良好2例，中残4例，重残3例，植物生存1例，死亡3例。结论颅脑外伤术后可随时发生大面积脑梗死．致死、致残率高。对此，术后应及时复查CT，对大面积脑梗死应早期发现，充分减压，及早采用综合治疗以提高疗效。     

高龄大面积脑梗死的综合治疗临床观察

目的 :观察以脑保护为主的综合疗法对高龄大面积梗死的疗效。方法 :将 6 0岁以上经头颅 CT或 MRI确诊为大面积脑梗死患者分为综合治疗组 2 8例 ,对照组 2 6例 ,比较两组疗效。结果 :综合治疗组总有效率 82 .14 % ,明显高于对照组 4 2 .31% (P <0 .0 1) ;死亡率治疗组 7.14 % ,对照组 2 6 .93% ;治疗组治疗前后血液流变学指标及血脂比较有显著性差异 (P <0 .0 5 )。结论 :综合治疗可显著改善高龄大面积脑梗死患者的预后     

恩必普治疗大面积脑梗死临床观察

目的 观察恩必普治疗大面积脑梗死的临床疗效.方法 55例大面积脑梗死患者随机分为观察组33例和对照组22例,对照组应用常规治疗,观察组在对照组的基础上加用恩必普,14d一疗程,对2组患者在入院时及第14、28d各进行神经功能缺损程度评分及复查头颅CT,并同时进行疗效评定.结果 2组病人14、28d神经功能缺损程度评分均较治疗前明显好转(P<0.05),观察组总有效率90.91%优于对照组的72.73%,差异有统计学意义(P<0.05);且观察组脑梗死面积在治疗后缩小较对照组明显(P<0.01).结论 恩必普治疗大面积脑梗死能有效改善神经功能缺损且疗效显著,并能缩小脑梗死面积.     

Environmental factors in the development and progression of late-onset Alzheimer＇s disease

Late-onset Alzheimer＇s disease （LOAD） is an age-related neurodegenerative disorder characterized by gradual loss of synapses and neurons, but its pathogenesis remains to be clarified. Neurons live in an environment constituted by neurons themselves and glial cells. In this review, we propose that the neuronal degeneration in the AD brain is partially caused by diverse environmental factors. We first discuss various environmental stresses and the corresponding responses at different levels. Then we propose some mechanisms underlying the specific pathological changes, in particular, hypothalamic-pituitary adrenal axis dysfunction at the systemic level; cerebrovascular dysfunction, metal toxicity, glial activation, and Aβ toxicity at the intercellular level; and kinase-phosphatase imbalance and epigenetic modification at the intracellular level. Finally, we discuss the possibility of developing new strategies for the prevention and treatment of LOAD from the perspective of environmental stress. We conclude that environmental factors play a significant role in the development of LOAD through multiple pathological mechanisms.     

大囊型脑囊虫病的诊断与治疗

目的 探讨大囊型脑囊虫病的临床特点和最佳治疗方法.方法 回顾性分析住院确诊的5例大囊型脑囊虫病的临床特点、影像学检查和治疗方法.结果 大囊型脑囊虫病颅内压增高不明显;MRI平扫及增强大囊泡寄生部位散在脑实质及小脑,囊泡呈圆形或类圆形,个别有分叶,囊壁薄而规则,大囊呈长T1长T2信号,增强扫描3例表现为囊壁呈环状轻度强化、2例无强化;2例外科手术治疗,2例吡喹酮和阿苯达唑联合治疗,1例吡喹酮治疗无效加用阿苯达唑明显见效.结论 大囊型脑囊虫病临床及影像学有特征性改变;药物治疗是根本;阿苯达唑对于大囊型脑囊虫病疗效好.     

高血压脑出血的显微外科治疗进展

高血压脑出血（Hypertensive intrac-rebral hemorrhage,HICH）是具有高发病率、高病死率、高致残率的急性脑血管疾病,占所有脑卒中患者的10%-20%,早期病死率可高达49.4%。随着人口老龄化,其发病率逐年提高;而外科手术的干预,使其病死率有所下降,但致残率居高不下。如何提高手术疗效和患者生存质量,一直是神经外科医师努力的方向。微侵袭血肿清除术因其手术创伤小,恢复快,是目前国内治疗高血压脑出血的重要手段。     

神经内镜联合亚低温治疗高血压基底节区脑出血

目的 探讨神经内镜联合亚低温在治疗高血压基底节区脑出血中的临床应用价值.方法 回顾性分析我院神经内镜治疗高血压基底节区脑出血患者40例的临床资料,并对治疗结果进行分析.结果 神经内镜治疗组22例(甲组),神经内镜联合亚低温治疗组18例(乙组),术后3个月根据GCS评分,甲组恢复良好1例,中残4例,重残6例,植物生存6例,死亡5例;乙组恢复良好4例,中残8例,重残3例,植物生存1例,死亡2例,两组比较差异有统计学意义(P＜0.05).两组颅内压比较第1天两者差异不明显,但第2、3天亚低温组颅内压明显降低.结论 神经内镜是治疗高血压基底节区脑出血较为有效的手术方式,联合亚低温治疗能有效降低颅内压,改善术后神经功能恢复,具有较好的临床应用价值.     

阿尔茨海默病治疗的研究进展

阿尔茨海默病（AD）是一种隐匿性起病,进行性恶化的神经退行性疾病,临床最初表现为认知功能障碍,并有可能在5～10年内完全衰退。患者往往伴随严重的记忆力丧失、精神行为异常、人格改变、言语功能障碍,无法独立生活,最终近乎于植物状态。Ferri等采用DISMOD软件在全球60岁以上人群中估计,全球的痴呆患者人数到2040年将达到8llO万左右。     

Effects of p75 neurotrophin receptor knockout on axonal regeneration in a mouse model of facial nerve injury

BACKGROUND： Previous studies have shown that p75 neurotrophin receptor plays an important role in peripheral nerve injury. However, the role of p75 neurotrophin receptor in the regeneration of peripheral nerves remains poorly understood. OBJECTIVE： To study the effect of p75 neurotrophin receptor on facial nerve regeneration. DESIGN, TIME AND SETTING： A randomized controlled experiment was performed in the Regeneration Laboratory of Flinders University, Australia and the Biomedical Laboratory of Dentistry School, Shandong University from March 2005 to February 2006. MATERIALS： Cholera toxin B subunit, fast blue, and biotin rabbit-anti goat IgG were provided by Sigma, USA; goat-anti choleratoxin B subunit ant/body was provided by List Biologicals, USA. METHODS： In p75 neurotrophin receptor knockout and wild type 129/sv mice, the facial nerves on one side were crushed. At days 2 and 4 following injury, regenerating motor neurons in the facial nuclei were labeled by fast blue, and the regenerating axon was labeled by the anterograde tracer choleratoxin B subunit. MAIN OUTCOME MEASURES： Axonal regenerative velocity and number were detected by immunohistochemical staining of choleratoxin B subunit, growth-associated protein, protein gene product 9.5, and calcitonin-gene-related peptide; survival of motor neurons in the facial nuclei was detected by retrograde fast blue. RESULTS： Axonal growth in the facial nerve of p75 neurotrophin receptor knockout mice was significantly less than in wild type mice. At day 7 after injury, the number of regenerating motor neurons in p75 neurotrophin receptor knockout mice remained significantly less than in wild type mice （P 〈 0.05）. The number of positively stained fibers for growth-associated protein-43, protein gene product 9.5, and calcitonin-gene-related peptide in p75 neurotrophin receptor knockout mice was significantly less than in wild type mice （P 〈 0.01）. CONCLUSION： p75 neurotrophin receptor promoted axonal regeneration and enhanced the survival rate of motor neurons following facial nerve injury.     

微创手术治疗慢性硬膜下血肿的临床分析

目的 总结分析微创引流手术(使用YL-1型一次性颅内血肿穿刺粉碎针)联合尿激酶技术治疗慢性硬膜下血肿的效果.方法 对48例慢性硬脑膜下血肿患者根据头颅CT扫描结果,采用局部麻醉下微创血肿腔置入YL-1型一次性颅内血肿穿刺粉碎针引流,若血肿中有血凝块,则分次血肿腔注入尿激酶溶解血肿液引流的方法治疗.并对治愈出院患者进行随访,总结治疗效果.结果 48例患者均获得随访,平均随访3个月,全组患者均取得较满意治疗效果,与手术相关并发症发生率为 2.08％(1/48),为非张力性气颅1例.结论 采用微创引流手术(使用YL-1型一次性颅内血肿穿刺粉碎针)联合尿激酶技术治疗慢性硬膜下血肿,能取得较钻孔引流术单纯微创冲洗引流更好的治疗效果.     

Edema and neuronal apoptosis in the hippocampus and cortex of elderly rats following transient cerebral ischemia/reperfusion injury

BACKGROUND： Previous studies of cerebral ischemia have used young animals, with an ischemic time greater than 5 minutes （safe time limit）. Despite an increased understanding of neuronal apoptosis, it remains uncertain whether brief cerebral ischemic events of 5 minutes or less damage brain tissue in elderly rodents. OBJECTIVE： To investigate the effects of transient cerebral ischemia （5 minutes）/reperfusion injury on brain cortical and hippocampal edema, aquaporin-4 （AQP-4） expression, and neuronal apoptosis in aged rats, and to compare ischemic sensitivity between cortex and hippocampus. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Institute of Cerebrovascular Disease, Qingdao University Medical School from April 2008 to March 2009. MATERIALS： Rabbit anti-AQP-4 polyclonal antibody, TUNEL kit, and SABC immunohistochemistry kit were purchased from Wuhan Boster Bioengineering, China. METHODS： A total of 160 healthy, male, aged 19-21 months, Wistar rats were randomly assigned to 4 groups： sham-surgery, and ischemia 1-, 3-, and 5-minute groups, with 40 rats in each group. The global cerebral ischemia model was established using the Pusinelli four-vessel occlusion, and the three cerebral ischemia groups were subdivided into reperfusion 12-hour, 1-, 2-, 3-, and 7-day subgroups, with 8 rats in each subgroup. The sham-surgery group was subjected to exposure of the first cervical bilateral alar foramina and bilateral common carotid arteries. MAIN OUTCOME MEASURES： The dry-wet weight assay was used to measure brain water content and histopathology of the cortex and hippocampus was observed following hematoxylin-eosin staining. In addition, cortical and hippocampal AQP-4 expression was detected by streptavidin-biotin complex immunohistochemistry, and neuronal apoptosis was detected by the TUNEL method. RESULTS： There was no significant difference in brain water content or AQP-4 expression in the cortex and hippocampus between ischemia 1- and 3-minute groups and the sham-surgery group or brain water content or AQP-4 expression in the cortex between ischemia 5-minute group and sham-surgery group （P 〉 0.05）. However, brain water content and AQP-4 expression in the hippocampus after 5 minutes of cerebral ischemia were significantly increased compared with the sham-surgery group （P 〈 0.05 or P 〈 0.01）. Several TUNEL-positive cells were observed in the cortex and hippocampus of the sham-surgery group and ischemia 1-minute group, as well as in the cortex of the ischemia 3-minute group. In addition, the number of apoptotic neurons in the hippocampus of ischemia 3-minute group and in the cortex and hippocampus of ischemia 5-minute group was significantly increased （P 〈 0.05 or P 〈 0.01 ）. Neuronal apoptosis was increased after 12 hours of ischemia/reperfusion, and it reached a peak by 2 days （P 〈 0.01）. CONCLUSION： Transient cerebral ischemia （5 minutes） resulted in increased hippocampal edema, AQP-4 expression, and neuronal apoptosis. Moreover, cerebral ischemia had a greater effect on neuronal apoptosis than brain edema or AQP-4 expression, and the hippocampus was more sensitive than the cortex.     

Dysfunctional autophagy in Alzheimer＇s disease： pathogenic roles and therapeutic implications

Neuronal autophagy is essential for neuronal survival and the maintenance of neuronal homeostasis. Increasing evidence has implicated autophagic dysfunction in the pathogenesis of Alzheimer＇s disease （AD）. The mechanisms underlying autophagic failure in AD involve several steps, from autophagosome formation to degradation. The effect of modulating autophagy is context-dependent. Stimulation of autophagy is not always beneficial. During the implementation of therapies that modulate autophagy, the nature of the autophagic defect, the timing of intervention, and the optimal level and duration of modulation should be fully considered.