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视神经血管母细胞瘤一例
患者男,45岁.主因"无明显诱因左眼视力下降半年,视力丧失",于2004年6月3日入我院.曾在当地按"视盘血管炎"给予对症治疗,无明显疗效.体检:左眼视力无光感.眼球突出度:右眼15 mm,左眼15 mm.眶距105 mm.眼球运动、眼压及眼前节检查正常.直接光反射消失,间接光反射存在.眼底检查:视盘水肿,色淡,视盘上方少许渗出,黄斑中心反射消失.标准化A/B超、CT、MRI检查显示左视神经增粗,视神经内中部可见一圆形占位病变.临床诊断:左视神经增粗原因待查,视神经内肿物?入院后全身检查未见异常.患者于全麻下行左外侧开眶术,术中见视神经增粗,包膜光滑.切开鞘膜有透明清亮液体溢出,直视下切除球后视神经约2 cm,常规骨瓣固定,缝合.
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新生儿视神经缺损一例
先天性视神经乳头缺损常单眼发病.本病为胚胎时眼泡胚胎闭合不全所致,常伴有脉络膜缺损,而仅有视盘缺损则少见[1].患者多因视觉发育期出现视力不良、斜视、眼球震颤等症状时才得以发现.新生儿期就发现视神经缺损未见报道,我们经新生儿眼病筛奋发现的1例,现报道如下.
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Non-arteritic anterior ischemic optic neuropathy (NA-AION) is the most common cause of acute ischemic damage to the optic nerve (ON), and the leading cause of seriously impaired vision in people over 55 years of age. It demonstrated that subcutaneous administration of Granulocyte colony-stimulating factor (G-CSF) reduces RGC death in an ON crush model in rats, and that the neuroprotective effects may involve both anti-apoptotic and anti-inlfammatory processes. Our recent work shows that the protective actions of G-CSF in rAION models may involve both anti-apoptotic and anti-inlfammatory processes. However, the exact rescuing mech-anisms involved in the administration of G-CSF in rAION models need further investigation. In addition, further studies on the administration of G-CSF at different time intervals after the induction of rAION may be able to illustrate whether treatment given at a later time is still neu-roprotective. Further, it is unknown whether treatment using G-CSF combined with other drugs will result in a synergistic effect in a rAION model. Inlfammation induced by ischemia plays an essential role on the ON head in NA-AION, which can result in disc edema and compartment changes. Therefore, it is reasonable that adding an anti-inflammatory drug may enhance the therapeutic effects of G-CSF. An ongoing goal is to evaluate the novel sites of action of both G-CSF and other anti-inlfammatory drugs, and to identify the functionally protective pathways to enhance RGC survival. These investigations may open up new therapeutic avenues for the treatment of ischemic optic neuropathy.
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Secondary degeneration occurs commonly in the central nervous system after traumatic injuries and following acute and chronic diseases, including glaucoma. A constellation of mechanisms have been shown to be associated with secondary degeneration including apoptosis, necrosis, autophagy, oxidative stress, excitotoxicity, derangements in ionic homeostasis and calcium influx. Glial cells, such as microglia, astrocytes and oligodendrocytes, have also been demon-strated to take part in the process of secondary injury. Partial optic nerve transection is a useful model which was established about 13 years ago. The merit of this model compared with other optic nerve injury models used for glaucoma study, including complete optic nerve transection model and optic nerve crush model, is the possibility to separate primary degeneration from secondary degeneration in location. Therefore, it provides a good tool for the study of secondary degeneration. This review will focus on the research progress of the mechanisms of secondary degeneration using partial optic nerve transection model.
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Molecular mechanisms of the Kr?uppel-like family of transcription factors (KLFs) have been studied more in proliferating cells than in post-mitotic cells such as neurons. We recently found that KLFs regulate intrinsic axon growth ability in central nervous system (CNS) neurons in-cluding retinal ganglion cells, and hippocampal and cortical neurons. With at least 15 of 17 KLF family members expressed in neurons and at least 5 structurally unique subfamilies, it is import-ant to determine how this complex family functions in neurons to regulate the intricate genetic programs of axon growth and regeneration. By characterizing the molecular mechanisms of the KLF family in the nervous system, including binding partners and gene targets, and comparing them to deifned mechanisms deifned outside the nervous system, we may better understand how KLFs regulate neurite growth and axon regeneration.
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视神经损伤后节细胞的保护和神经修复的研究进展
高眼压、炎性病变、创伤、缺血及肿瘤压迫等均能严重损伤视神经,造成视力严重丧失.自1928年Cajal断言哺乳动物的中枢神经系统无再生能力以来,人们一直认为视神经损害后无法再生或修复.
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1例系统性红斑狼疮并发双眼视神经脱髓鞘病人的护理
系统性红斑狼疮(systemic lupus erythematosus,SLE)是累及全身多系统、多器官的自身免疫性疾病.病程迁延,病情反复发作,临床上主要表现为皮肤、关节和脏器损害,SLE以年轻女性多见,其中育龄妇女占90%~95%.
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睫状神经营养因子与生长相关蛋白-43在视神经损伤修复中作用
人类和其他成年哺乳动物的成熟中枢神经系统损伤后由于内在因素轴突很难再生,功能不可逆性丧失[1].视神经作为中枢神经的一部分,由于解剖上的易及性及其他特性,许多中枢神经系统损伤再生的研究将视神经作为经典实验模型[1].
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人类线粒体基因突变与Leber遗传性视神经病变
Leber遗传性视神经病变是一种罕见的典型母系遗传的致盲性视神经变性眼部疾病,由Von Graefe 1858年首次报道,1871年德国眼科医生Theodor Leber首次描述了这种遗传性眼病,主要表现为双眼急性或亚急性中心视力下降,多累及青年男性,随后便将此病命名为Leber遗传性视神经病变,后又称为Leber视神经炎、Leber视神经萎缩、遗传性视神经萎缩、遗传性球后视神经炎等等.