蛛网膜囊肿合并慢性硬膜下血肿1例并文献复习

目的 总结颅内蛛网膜囊肿合并慢性硬膜下血肿的诊治经验。方法 回顾性分析1例右侧外侧裂池蛛网膜囊肿合并复发性慢性硬膜下血肿的临床资料，并结合相关文献进行分析。结果 首次按传统慢性硬膜下血肿治疗方式，行右侧颞部钻孔引流，术后3周血肿复发；再次行开颅血肿清除术+蛛网膜囊肿切除术，术后恢复良好，随访10个月，血肿无复发。结论 对于蛛网膜囊肿合并慢性硬膜下血肿，有明显临床症状者需手术治疗，对于单纯硬膜下血肿，可行钻孔引流术；若合并囊内出血，建议开颅手术，有利于改善病人预后。     

儿童颅内幕上蛛网膜囊肿的手术治疗

目的总结儿童颅内幕上蛛网膜囊肿手术治疗的经验。方法回顾性分析56例幕上蛛网膜囊肿病儿的临床资料,均经手术治疗,手术方法包括囊肿壁部分切除加囊肿脑池交通术30例,囊肿壁部分切除并囊肿脑池交通加颞肌条填入术20例,囊肿-腹腔分流术5例及神经内镜下囊肿壁部分切除并造瘘术1例。结果病儿术后临床症状均不同程度改善,颅内压增高症状术后均消失。术后高热(39℃)12例,并发颅内血肿4例,无手术死亡。随访3个月～5年,囊肿消失18例,缩小80%以上22例,缩小50%～80%8例,无明显变化6例;2例合并脑积水者,1例脑室较术前略缩小,另1例无变化。结论外科手术是儿童颅内幕上蛛网膜囊肿的有效治疗方法,术中仔细和轻柔操作是预防和减少相关手术并发症的关键。     

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.     

儿童颅内蛛网膜囊肿的外科治疗探讨

目的 探讨儿童颅内蛛网膜囊肿外科治疗的手术方法、适应证及并发症.方法 回顾分析53例手术患儿的临床资料,囊肿切除并脑池交通术42例,囊肿-腹腔分流术10例,神经内镜下囊肿切除并造瘘术1例.结果 患者术后恢复均良好,临床症状均有不同程度改善.术后高热(>39.1℃)及持续发热(>3d)13例;形成皮下积液8例,再次硬膜修补术2例.术后随访3个月以上,CT证实囊肿缩小或消失50例,无明显变化3例.结论 上述三种术式均是治疗儿童颅内蛛网膜囊肿的有效方案,但应综合多种因素采取个体化的治疗,并重视预防其相关术后并发症.     

经颅穿刺治疗慢性硬膜下血肿72例体会

目的探讨经颅穿刺治疗慢性硬膜下血肿的方法和疗效。方法经CT引导定位,采用适当长度（约20mm）YL-I型颅内血肿穿刺针,钻孔冲洗引流慢性硬膜下血肿,并闭式引流。结果72例患者共行经颅穿刺术78部位次;术后全部病例临床症状迅速改善,意识障碍和偏瘫症状好转,术后复查CT,硬膜下血肿全部清除53例,硬膜下腔残留低密度少量积液19例,其中6例表现为脑脊液引流症状,经治疗后痊愈,未发生张力性气颅、颅内血肿、颅内感染和癫痫发作等并发症。术后随访3个月未见血肿复发病例。结论CT引导下经颅穿刺治疗慢性硬膜下血肿操作简便,创伤较小,并发症少,是一种安全有效的微侵袭治疗技术。     

单颅孔钻孔冲洗结合单管闭式引流治疗慢性硬膜下血 肿简

目的探讨单颅孔钻孔冲洗结合单管闭式引流治疗慢性硬膜下血肿的有效性及可行性。方法回顾性分析58例慢性硬膜下血肿病人的临床资料及手术治疗情况。结果本组恢复良好52例（89．7％）,术后发生术侧急性硬膜外血肿2例,同侧急性硬膜下血肿1例,血肿复发2例,切口感染1例。所有病人出院后随访2个月～2年,无血肿复发。结论对慢性硬膜下血肿病人．单颅孔钻孔冲洗结合单管闭式引流是一种安全、有效的手术方式。     

慢性硬膜下血肿钻孔引流术及并发症的防治

目的对52例慢性硬膜下血肿的钻孔引流治疗及并发症进行研究和探讨。方法 52例慢性硬膜下血肿均行钻孔引流术。结果治愈48例(92.3%),无死亡病例,颅内积气较多4例(含1例张力性气颅),脑内血肿1例,血肿复发2例,癫发作1例及脑脊液漏1例。结论了解慢性硬膜下血肿术后并发症的原因,积极采取措施对症处理,可有效预防并发症的发生。     

微创穿刺术治疗慢性硬膜下血肿45例分析

目的观察微创穿刺术治疗慢性硬膜下血肿。方法使用YL-1型颅内血肿粉碎穿刺针进行45例慢性硬膜下血肿手术治疗的疗效观察。结果慢性硬膜下血肿患者经微创术穿刺血肿冲洗引流2～3d后,血肿完全或大部分清除,脑受压消失。结论微创术是治疗慢性硬膜下血肿的一种更简便、安全有效、经济的治疗方法。     

锥颅微创置管引流术治疗慢性硬膜下血肿40例

目的探讨慢性硬膜下血肿的发病机制及治疗。方法总结40例经锥颅微创置管引流术治疗的慢性硬膜下血肿病人的临床资料,从临床表现、疗效及并发症等方面进行分析。结果本组平均手术时间(0.5±0.3)h,术中平均出血量(15±5)ml,平均住院时间(6±2.1)d。40例术后复查颅脑CT,硬膜下血肿均达大部分清除。术后并发颅内积气6例,硬膜外血肿1例,硬膜下积液5例,颅内感染1例。40例病人随访3个月,血肿复发1例,未见新增神经功能障碍。结论锥颅微创置管引流术治疗慢性硬膜下血肿手术时间和住院时间短,术后并发症少,具有一定的临床价值。     

儿童蛛网膜囊肿破裂继发慢性硬膜下血肿分析(附二例报告)

颅内蛛网膜囊肿是儿童常见的一种先天性颅内良性病变,是儿童发生慢性硬膜下血肿的危险因素[1].我科收治2例儿童颅内蛛网膜囊肿外伤性破裂形成硬膜下积液继发慢性硬膜下血肿的病例,现报告如下.     

Ultrastructure of non-myelinated neurons during energy deprivation

Summary This paper examines the neuropathology of oxygen-glucose deprivation uncomplicated by stagnant conditions. Rabbit vagus nerves were pulled into asmulti-compartment perfusion chamber, stimulated five times per second and deprived of energy by substituting nitrogen and deoxyglucose for oxygen and glucose in the Locke's perfusate. After incubation the compartments were perfused with gluteraldehyde solution, and the nerves were prepared for electron microscopy. Fixation in the compartments ensured precise cross and longitudinal sections which permitted quantitative comparisons. Although the action potentials ceased in 45 min, 1 h of energy deprivation did not significantly affect the ultrastructure. After 2 h of deprivation the axons were smaller and flattened and microtubules appeared packed together. In the smallest axons the microtubules were gone, the neurofilaments were compacted and the few mitochondria had a dense, homogenous appearance. By 4 h the shrinking was extreme, yet 8% were swollen much larger than any of the controls. Longitudinal views showed these balloned areas were greatly expanded regions of the smallest axons. Both tiny and huge regions were devoid of microtubules and the swollen axons contained expanded mitochondria.Calcium is indirectly implicated in the pathogenesis by the concurrence of mitochondrial alteration as the microtubules disappear coupled with the known role of mitochondria in calcium regulation and the reported effect of high calcium on microtubual dissociation. In is suggested that axons first shrink as osmotially active molecules are used or washed out. After a time without energy the mitochondria can no longer regulate the intracellular calcium, microtubules dissociate, and calcium-activated phospholipases create osmotically active molecules. Finally, high-amplitude, disruptive swelling occurs.Supported, in part, by a Grant-in-aid from the American Heart Association with funds contributed by the American Heart Association, Kansas Affiliate and by the University of Kansas Biomedical Sciences Support Grant RR0737     

星形胶质细胞对天冬氨酸特异性半胱氨酸蛋白酶介导β淀粉样蛋白早期突触毒性作用的影响

目的探讨星形胶质细胞(astrocyte,AS)对天冬氨酸特异性半胱氨酸蛋白酶(cysteinyl aspartate specific proteinase,caspase)介导β淀粉样蛋白(β-amyloid,Aβ)早期突触毒性作用的影响,以期为进一步研究与血管性痴呆(vascular dementia,Va D)的发病机制奠定基础。方法以原代培养大鼠海马纯神经元体系(NE-S)及混合培养体系(MIX-S,主要包含神经元及AS)为研究对象,各体系分为6组:对照组、caspase-8抑制剂组、caspase-9抑制剂组、Aβ处理组、caspase-8抑制剂预处理加Aβ组和caspase-9抑制剂预处理加Aβ组。免疫荧光检测各组近胞体10μm段树突中突触后密度蛋白(postsynaptic density-95,PSD95)表达量的变化。结果 1在NE-S与MIX-S中,与对照组相比,caspase-8抑制剂组、caspase-9抑制剂组PSD95的表达量均无明显差异,Aβ处理组PSD95的表达量均显著降低(P均0.001)。2在NE-S中,与Aβ处理组相比,caspase-9抑制剂预处理加Aβ组PSD95的表达量显著回升至对照组水平,caspase-8抑制剂预处理加Aβ组则无显著改变;在MIX-S中的结果则相反,即caspase-8抑制剂预处理加Aβ组PSD95的表达量显著回升至对照组水平,而caspase-9抑制剂预处理加Aβ组则无显著改变。3MIX-S与NE-S两种培养系统间相比较,对照组间及Aβ处理组间PSD95的表达量均无显著差异,而caspase-8抑制剂预处理加Aβ组间及caspase-9抑制剂预处理加Aβ组间PSD95的表达量差异有显著性。结论在Aβ早期突触毒性作用中,AS参与caspase-8介导的死亡受体通路激活过程,且参与抑制神经元的线粒体通路。     

Effects of genistein on neuronal apoptosis, and expression of Bcl-2 and Bax proteins in the hippocampus of ovariectomized rats

Genistein is one of several isoflavones that has a structure similar to 17β-estradiol, has a strong antioxidant effect, and a high affinity to estrogen receptors. At 15 weeks after ovariectomy, the expression of Bcl-2 in the hippocampus of rats decreased and Bax expression increased, with an obvious upregulation of apoptosis. However, intraperitoneal injection of genistein or 17β-estradiol for 15 consecutive weeks from the second day after operation upregulated Bcl-2 protein expression downregulated Bax protein expression, and attenuated hippocampal neuron apoptosis. Our experimental findings indicate that long-term intervention with genistein can lead to a decrease in apoptosis in hippocampal neurons following ovariectomy, upregulate the expression of Bcl-2, and downregulate the expression of Bax. In addition, genistein and 17β-estradiol play equal anti-apoptotic and neuroprotective roles.     

Magnetic resonance morphometry of the loss of gray matter volume in Parkinson’s disease patients

Voxel-based morphometry can be used to quantitatively compare structural differences and functional changes of gray matter in subjects.In the present study,we compared gray matter images of 32 patients with Parkinson’s disease and 25 healthy controls using voxel-based morphometry based on 3.0 T high-field magnetic resonance T1-weighted imaging and clinical neurological scale scores.Results showed that the scores in Mini-Mental State Examination and Montreal Cognitive Assessment were lower in patients compared with controls.In particular,the scores of visuospatial/executive function items in Montreal Cognitive Assessment were significantly reduced,but mean scores of non-motor symptoms significantly increased,in patients with Parkinson’s disease.In addition,gray matter volume was significantly diminished in Parkinson’s disease patients compared with normal controls,including bilateral temporal lobe,bilateral occipital lobe,bilateral parietal lobe,bilateral frontal lobe,bilateral insular lobe,bilateral parahippocampal gyrus,bilateral amygdale,right uncus,and right posterior lobe of the cerebellum.These findings indicate that voxel-based morphometry can accurately and quantitatively assess the loss of gray matter volume in patients with Parkinson’s disease,and provide essential neuroimaging evidence for multisystem pathological mechanisms involved in Parkinson’s disease.     

Development of 18F-labeled radiotracers for neuroreceptor imaging with positron emission tomography

Positron emission tomography (PET) is an in vivo molecular imaging tool which is widely used in nuclear medicine for early diagnosis and treatment follow-up of many brain diseases. PET uses biomolecules as probes which are labeled with radionuclides of short half-lives, synthesized prior to the imaging studies. These probes are called radiotracers. Fluorine-18 is a radionuclide routinely used in the radiolabeling of neuroreceptor ligands for PET because of its favorable half-life of 109.8 min. The delivery of such radiotracers into the brain provides images of transport, metabolic, and neurotransmission processes on the molecular level. After a short introduction into the principles of PET, this review mainly focuses on the strategy of radiotracer development bridging from basic science to biomedical application. Successful radiotracer design as described here provides molecular probes which not only are useful for imaging of human brain diseases, but also allow molecular neuroreceptor imaging studies in various small-animal models of disease, including genetically-engineered animals. Furthermore, they provide a powerful tool for in vivo pharmacology during the process of pre-clinical drug development to identify new drug targets, to investigate pathophysiology, to discover potential drug candidates, and to evaluate the pharmacokinetics and pharmacodynamics of drugs in vivo.     

Differential expression of carboxyl terminal derivatives of amyloid precursor protein among cell lines.

Understanding the pathway for amyloid percursor protein (APP) catabolism has become an important line of investigation. APP is a ubiquitous membrane bound protein that is rapidly cleaved at the membrane, yielding a secreted protein identical to protease nexin II and an internalized 11.5 kDa 100 residue C terminal derivative (CTD). The levels of CTDs in a variety of cell lines have been examined and were found to differ. Cell types associated with the pathology of Alzheimer's disease (AD), such as olfactory neuroblasts (ON) and cortical vascular endothelial cells, have higher levels of CTDs than lymphoblasts and melanoma cells. The mechanism of CTD catabolism appears to involve the lysosome because blockade of lysosomal but not endosomal or mitochondrial function results in increased levels of CTDs. Under these conditions, production of larger, amyloidogenic CTDs is also seen. In cells possessing higher levels of CTDs we find that the mechanism for production of amyloidogenic CTDs may involve the internalization of intact full-length APP. Thus, inhibition of the lysosomal system appears capable of generating amyloidogenic peptides. The amount of amyloidogenic peptides appears to vary among cell lines. Such variation may shed light on why amyloid accumulates around specific cell types such as vascular endothelial cells, neurons, and glia. Finally, disfunction of the lysosomal system may play a role in the pathogenesis of Alzheimer's disease.     

Neuroprotective role of fibronectin in neuron-glial extrasynaptic transmission

Most hypotheses concerning the mechanisms underlying Parkinson’s disease are based on altered synaptic transmission of the nigrostriatal system.However,extrasynaptic transmission was recently found to affect dopamine neurotransmitter delivery by anisotropic diffusion in the extracellular matrix,which is modulated by various extracellular matrix components such as fibronectin.The present study reviewed the neuroprotective effect of fibronectin in extrasynaptic transmission.Fibronectin can regulate neuroactive substance diffusion and receptor activation,and exert antineuroinflammatory,adhesive and neuroprotective roles.Fibronectin can bind to integrin and growth factor receptors to transactivate intracellular signaling events such as the phosphatidylinositol 3-kinase/protein kinase B pathway to regulate or amplify growth factor-like neuroprotective actions.Fibronectin is assembled into a fibrillar network around cells to facilitate cell migration,molecule and ion diffusion,and even drug delivery and treatment.In addition,the present study analyzed the neuroprotective mechanism of fibronectin in the pathogenesis of Parkinson’s disease,involving integrin and growth factor receptor interactions,and discussed the possible therapeutic and diagnostic significance of fibronectin in Parkinson’s disease.     

Clinical and molecular research of neuroacanthocytosis

Neuroacanthocytosis is an autosomal recessive or dominant inherited disease characterized by widespread, non-specific nervous system symptoms, or spiculated "acanthocytic" red blood cells. The clinical manifestations typically involve chorea and dystonia, or a range of other movement disorders. Psychiatric and cognitive symptoms may also be present. The two core neuroacanthocytosis syndromes, in which acanthocytosis is atypical, are autosomal recessive chorea-acanthocytosis and X-linked McLeod syndrome. Acanthocytes are found in a smaller proportion of patients with Huntington’s disease-like 2 and pantothenate kinase-associated neurodegeneration. Because the clinical manifestations are diverse and complicated, in this review we present features of inheritance, age of onset, neuroimaging and laboratory findings, as well as the spectrum of central and peripheral neurological abnormalities and extraneuronal involvement to help distinguish the four specific syndromes.     

轻型缺血性卒中静脉溶栓后双重抗血小板疗效观察

目的 观察rt-PA静脉溶栓联合双重抗血小板治疗轻型缺血性卒中的有效性及安全性。 方法 以2013年12月-2016年12月在石家庄市第一医院连续住院治疗的轻型缺血性卒中患者为研究 对象,将其随机分为对照组、溶栓+单抗组和溶栓+双抗组。对照组不进行静脉溶栓,长期口服阿 司匹林（100 mg/d）抗血小板治疗;溶栓+单抗组在rt-PA静脉溶栓（0.9 mg/kg,最大剂量90 mg）基 础上长期单用阿司匹林（100 mg/d）抗血小板治疗;溶栓+双抗组在溶栓后单抗基础上加用氯吡格雷 （75 mg/d）双重抗血小板治疗,双抗治疗21 d后改为阿司匹林长期单抗治疗。随访3个月,有效性指标 为3个月时NIHSS 0～1分、Barthel指数（Barthel index,BI）95～100分和mRS 0～1分的比例,3个月时缺 血性卒中的复发率;安全性指标为治疗24 h出血转化和症状性出血转化的发生率。另外比较三组间 基线和3个月时血清hs-CRP和IL-6的水平差异。 结果 研究共纳入85例患者,对照组28例,溶栓+单抗组28例,溶栓+双抗组29例,全部患者均完 成3个月随访,无死亡患者。对照组、溶栓+单抗组和溶栓+双抗组3个月随访时NIHSS 0～1分比例分 别为46.43%、78.57%和93.10%,BI 95～100分比例分别为53.57%、82.14%和89.66%,mRS 0～1分 的比例分别为50.00%、82.14%和93.10%,三组上述有效性指标差异均有统计学意义,两两比较显 示,溶栓+双抗组高于溶栓+单抗组和对照组,溶栓+单抗组高于对照组,差异均有统计学意义;对 照组、溶栓+单抗组和溶栓+双抗组3个月时缺血性卒中复发率分别为32.14%、7.14%和3.45%,差异 有统计学意义。安全性指标方面,三组均无出血转化事件。对照组、溶栓+单抗组和溶栓+双抗组3 个月时的hs-CRP水平分别为11.92±3.58 mg/L、9.04±2.85 mg/L和6.04±2.65 mg/L,IL-6水平分别为 26.18±4.65 ng/L、16.11±6.93 ng/L和12.84±2.57 ng/L,三组上述炎症因子水平差异均有统计学意 义,其中溶栓+双抗组低于溶栓+单抗组和对照组,溶栓+单抗组低于对照组。 结论 对于急性轻型缺血性卒中患者,rt-PA静脉溶栓治疗后短期双重抗血小板治疗可显著改善患 者神经功能,降低炎症因子水平,降低复发率,且不增加出血风险。     

血浆甘油三酯水平与缺血性卒中出院结局关系研究

目的   探讨急性缺血性卒中患者入院时血浆甘油三酯（triglyceride,TG）水平与出院结局不良的关系。 方法  采用回顾性队列研究的方法,连续纳入内蒙古兴安盟人民医院2009年6月1日～2012年5月31日急性缺血性卒中患者,共计3351例。结局不良组定义为患者出院时改良Rankin量表（modified Rankin Scale,mRS）评分≥3分,对结局不良组和结局良好组患者间基线资料进行比较。用四分位数法将患者入院时血浆TG水平分为4组,用非条件Logistic回归分析入院时TG水平与急性缺血性卒中出院结局不良的关系,计算比值比（odds ratio,OR）及95%可信区间（confidence interval,CI）。 结果  研究对象中发生结局不良的共341例,发生率为10.2%。单因素非条件Logistic回归分析结果显示,TG相对最高分位数组（TG＞2.12?mmol/L）,第1、2、3分位数组（TG分别为≤1.06?mmol/L、1.06～1.46?mmol/L、1.46～2.12?mmol/L）的结局不良发生率差异有显著性（P＜0.001）。在调整了年龄、住院天数、发病到入院时间、缺血性卒中首发、吸烟、饮酒、心脏病史、心房颤动史、高血压、高血糖和心率后,相对于最高分位数组,第3分位数组的结局不良发生率差异无显著性（P=0.0758）,而第1、2分位数组结局不良发生率升高（均P＜0.0001）,其OR（95%CI）分别为11.883（1.307～2.714）和2.063（1.436～2.963）。 结论  急性缺血性卒中患者入院时低水平TG可能独立地增加出院结局不良的风险。