外伤性视神经病变的病理生理学与临床研究

发布时间：2018-06-02 14:51

本文选题：视神经损伤 + 视神经减压　；参考：《山西医科大学》2011年硕士论文

【摘要】：外伤性视神经病变(traumatic optic neuropathy TON)是常见的视神经损伤类型,近年发病率呈上升趋势。伤后视力损害严重,约50%的患者遗留永久性视力丧失。目前临床上使用糖皮质激素为主的药物治疗法和手术治疗法是最常用的治疗手段,鼻内镜下视神经管减压术已成为目前主要的手术治疗方法。本论文旨在探讨外伤性视神经损伤的损伤机制、诊治方式方法、手术时机、治疗原则及预后相关因素等,总结目前临床诊治方法、手段及疗效,为临床治疗方案的选择提供依据与参考。为此,我们进行了如下探讨：第一部分：外伤性视神经病变的临床分析研究评价手术治疗和药物治疗外伤性视神经病变,分析影响疗效的临床因素。研究2005年1月至2010年10月太原市中心医院临床诊断为外伤性视神经病变但无影像学诊断依据的患者的临床资料。86例患者根据视力情况不同,分为A、B两个级别组,每组分为单纯药物治疗组和联合手术治疗组。将视力分为无光感、有光感、眼前手动、眼前手动指数和能见标准视力表(0.02以上)5个级别。对患者进行随访3月,与入院视力进行比较,视力提高1个级别者为有效,提高两个级别及以上者为显著,视力无进步或者下降者为无效,观察视力恢复情况。得出以下结果： 1、伤后无光感患者中,药物组与联合手术组比较,两者之间差别有统计学意义(p=0.040),联合手术疗效优于药物治疗。 2、伤后有光感患者中,药物组与联合手术组比较,两者之间差别有统计学意义(p=0.030),联合手术疗效优于药物治疗。 3、接受手术患者中,伤后7天以内手术组与7天以后手术组比较,两者之间差别有统计学意义(p=0.029),7天以内手术组优于7天以后手术组。由此,得出结论： 1、无论外伤性视神经病变患者伤后有无光感,联合手术治疗的疗效均优于单纯药物治疗。 2、手术时间以伤后7天以内为佳,但即使受伤时间较长,也不应轻易放弃。 3、伤后无光感、有昏迷史是影响眼视力预后的危险因素,手术治疗是保护视力的有力措施。第二部分：外伤性视神经病变动物模型的建立与视神经病理生理学观察建立接近临床状态的TON动物模型,研究视神经损伤的力学原理、神经病理生理学改变,为临床诊疗提供理论依据。鼠头解剖,观察眼眶、颅底与视神经关系。以大鼠为研究对象,对崔志利等设计的视神经损伤方法进行重复并改进,用小号动脉阻血镊夹伤视神经,建立与临床较为接近的轻、重TON动物模型,观察致伤后瞳孔和直接对光反射,并行模式翻转视觉诱发电位检查,对正常和损伤视神经进行病理形态学观察。得出结果： 1、麻醉清醒后,所有致伤眼均表现为瞳孔散大、直接对光反射迟钝或消失。无脑挫伤、感染、眶壁骨折、意外死亡 2、模式翻转视觉诱发电位(PR-VEP)检查：A组轻度损伤后P波潜伏期延迟,波幅降低,幅值在正常值的50%以上。B组重度损伤后波形迅速变宽平,1d时P波幅值低于正常值的50%,7d后PR-VEP不能被引出,表现为波形失去应有形态,无规律,波幅低,有的甚至完全消失,接近水平,即“熄灭”状态。 3、病理学观察：对照眼：视神经纤维平行排列,紧密整齐,其间少量少突胶质细胞。损伤眼：伤后1d,视神经水肿,散在空泡样变,血管周围稍有渗出,未见明显少突胶质细胞(OLs)增生。伤后7d,空泡变性严重,OLs增生明显。伤后2周,视神经肿胀减轻,轴突分布稀疏,胶质细胞、神经间质纤维组织及厚壁小血管增生。伤后4周,视神经脱髓鞘变性严重,轴突裸露,大量增生的胶质细胞以及胶原组织形成胶质疲痕,神经直径缩小。B组表现较A组严重。分析结果,得出结论： 1、本实验成功建立了外伤性视神经病的动物模型,为进一步系统研究TON的机制,并为临床上视神经损伤患者的临床分型、确定治疗方案及预后评估提供理论依据。 2、视神经损伤后依次经过水肿、胶质细胞增生和萎缩三个阶段,水肿期即7d以内治疗效果好。 3、轻度损伤组伤后视神经病理形态学改变随时间推移损伤进行性加重,但视神经有一定传导功能;重度损伤组伤后视神经迅速出现不可逆性溃变,视神经传导功能迅速丧失。 4、PR-VEP与视神经的病理形态学改变有很好的相关性,可以作为临床治疗的指导。第三部分结论本研究在理论和临床实践的基础上对外伤性视神经病变的相关问题展开研究,相关的研究结论如下： (1)本研究在理论模型的基础上构造了适合本研究的外伤性视神经病的动物模型,并对模型进行了相关的理论与临床论证,通过相应的临床数据分析,形成了自身的研究体系,为后续研究打下了一定理论基础。 (2)无论外伤性视神经病变患者伤后有无光感,联合手术治疗的疗效均优于单纯药物治疗。 (3)在临床中,患者受伤时间直接影响最终的治疗效果,病患一周内接受治疗相对能取得临床主动性。 (4)视神经损伤后依次经过水肿、胶质细胞增生和萎缩三个阶段,水肿期即7d以内治疗效果好。 (5)视神经和PR-VEP的相关性可以作为临床病患诊治的指导理论,因为两者之间病变相关性较好。 (6)轻度损伤组伤后视神经病理形态学改变随时间推移损伤进行性加重,但视神经有一定传导功能;重度损伤组伤后视神经迅速出现不可逆性溃变,视神经传导功能迅速丧失。
[Abstract]:Traumatic optic neuropathy (traumatic optic neuropathy TON) is a common type of optic nerve injury. The incidence of traumatic optic nerve is on the rise in recent years. The visual impairment after injury is serious, and about 50% of the patients are left with permanent visual loss. Endoscopic decompression of optic canal has become the main operative method. This paper aims to explore the mechanism of traumatic optic nerve injury, the methods of diagnosis and treatment, the time of operation, the principle of treatment and the related factors, etc., and summarize the methods, methods and effects of the clinical diagnosis and treatment, and provide the basis and reference for the selection of the clinical treatment plan. For this reason, we have carried out the following discussion:
Part one: clinical analysis of traumatic optic neuropathy.
Evaluation of surgical treatment and drug treatment of traumatic optic neuropathy, and analysis of the clinical factors affecting the curative effect. From January 2005 to October 2010, the clinical data of patients diagnosed as traumatic optic neuropathy in Taiyuan Central Hospital of Taiyuan, but without imaging diagnosis, were divided into two groups of A and B according to the difference of visual acuity. Each group was divided into a single drug treatment group and a combined surgical treatment group. The visual acuity was divided into 5 levels, without light sensation, light sensation, eye hand manual, hand eye manual index and standard visual acuity chart (above 0.02). The patients were followed up in March, compared with admission eyesight, visual acuity was improved by 1 levels, and two levels and above were significantly increased. No improvement or decrease in vision was observed and visual recovery was observed.
The following results are obtained:
1, in patients without light perception after injury, the difference between the drug group and the combined operation group was statistically significant (p=0.040), and the combined operation was better than the drug treatment.
2, in patients with light perception after injury, the difference between the drug group and the combined operation group is statistically significant (p=0.030), and the combined operation is better than the drug treatment.
3, the operation group was compared with the operation group within 7 days after the injury, and the difference between the two groups was statistically significant (p=0.029), and the operation group was better than the operation group after 7 days in 7 days.
Thus, the conclusion is drawn.
1, no matter whether the patients with traumatic optic neuropathy have light perception after injury, the curative effect of combined operation is better than that of simple drug therapy.
2, the operation time is better than 7 days after injury, but even if the injury time is longer, it should not be easily abandoned.
3, no light perception after injury and history of coma are risk factors affecting the prognosis of visual acuity. Surgical treatment is a powerful measure to protect vision.
The second part: establishment of animal model of traumatic optic neuropathy and pathophysiology of optic nerve.
Objective to establish a TON animal model which is close to the clinical state, and to study the mechanical principles and neuropathophysiological changes of optic nerve injury, so as to provide a theoretical basis for clinical diagnosis and treatment.
The rat head was dissected to observe the relationship between the eye orbit, the skull base and the optic nerve. The rats were used to repeat and improve the methods of optic nerve injury designed by Cui Zhili and so on. The optic nerve was clamped with the trumpet artery forceps. The light, heavy TON animal model, which was closer to the clinic, was established. The pupil and direct reflection of light after injury were observed, and the parallel pattern reversal was observed. Visual evoked potential (VEP) examination was performed to observe the normal and injured optic nerves.
The results are as follows:
1, after the anaesthesia, all the injured eyes were characterized by pupillary dilatation, slow or disappearance of light reflex. No brain contusion, infection, orbital wall fracture, accidental death.
2, pattern reversal visual evoked potential (PR-VEP) examination: the latency of P wave in A group was delayed after mild injury, the amplitude of wave decreased, the amplitude of.B in group.B of the normal value increased rapidly after severe injury, and the amplitude of P amplitude was lower than 50% of normal value at 1D, and PR-VEP could not be elicited after 7d, which showed that the waveform lost its due form, irregular, low amplitude and some Or even disappear completely, near the level, that is, "extinguish".
3, pathological observation: the control eye: the optic nerve fibers were arranged in parallel, close and neatly, and a small amount of oligodendrocyte. The injured eye: 1D after injury, edema of the optic nerve, scattered in vacuoles like, a little exudation around the blood vessels, no obvious oligodendrocyte (OLs) hyperplasia. After injury, 7d, vacuolar degeneration is serious, and OLs hyperplasia is obvious. Optic nerve swelling after 2 weeks after injury. In 4 weeks after injury, the degenerative degeneration of the optic nerve was serious, the axon was exposed, a large number of glial cells and collagen tissue formed glial scar, and the.B group of the nerve diameter narrowing was more serious than that in the A group.
The results are analyzed and the conclusion is drawn.
1, the experimental animal model of traumatic optic neuropathy was successfully established in this experiment to further systematically study the mechanism of TON, and to provide a theoretical basis for the clinical classification of the patients with optic nerve injury, and to determine the treatment plan and the prognosis evaluation.
2, optic nerve injury is followed by three stages of edema, glial cell proliferation and atrophy. The edema period is less than 7d.
3, the pathological changes of optic nerve after injury in the mild injury group were aggravated with the time lapse, but the optic nerve had a certain conduction function, and the severe injury group had an irreversible degeneration of the optic nerve after injury, and the optic nerve conduction function was lost quickly.
4, PR-VEP has a good correlation with the pathomorphological changes of optic nerve, and can be used as a guide for clinical treatment.
The third part of the conclusion
On the basis of theory and clinical practice, this study has carried out research on the related problems of traumatic optic neuropathy.
(1) on the basis of the theoretical model, this study constructed an animal model of traumatic optic neuropathy suitable for this study, and carried out the relevant theoretical and clinical demonstration of the model. Through the corresponding clinical data analysis, it formed its own research system and laid a theoretical foundation for the follow-up research.
(2) whether there is light perception in patients with traumatic optic neuropathy, the effect of combined surgery is better than that of simple drug therapy.
(3) in clinical practice, the time of injury is directly related to the final treatment effect. The patients can receive clinical initiative within a week.
(4) after optic nerve injury, edema, glial cell proliferation and atrophy were followed in three stages. The edema period was less than 7d.
(5) the correlation between optic nerve and PR-VEP can be used as a guiding theory for the diagnosis and treatment of clinical diseases, because the correlation between them is relatively good.
(6) the pathologic morphological changes of the optic nerve after injury in the mild injury group were aggravated with the time lapse, but the optic nerve had certain conduction function. The severe injury group had an irreversible degeneration of the optic nerve after injury, and the optic nerve conduction function was lost quickly.
【学位授予单位】：山西医科大学
【学位级别】：硕士
【学位授予年份】：2011
【分类号】：R779.1

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