本文選題：視神經(jīng)損傷 + 視神經(jīng)減壓��； 參考：《山西醫(yī)科大學(xué)》2011年碩士論文

【摘要】：外傷性視神經(jīng)病變(traumatic optic neuropathy TON)是常見的視神經(jīng)損傷類型,近年發(fā)病率呈上升趨勢(shì)。傷后視力損害嚴(yán)重,約50%的患者遺留永久性視力喪失。目前臨床上使用糖皮質(zhì)激素為主的藥物治療法和手術(shù)治療法是最常用的治療手段,鼻內(nèi)鏡下視神經(jīng)管減壓術(shù)已成為目前主要的手術(shù)治療方法。本論文旨在探討外傷性視神經(jīng)損傷的損傷機(jī)制、診治方式方法、手術(shù)時(shí)機(jī)、治療原則及預(yù)后相關(guān)因素等,總結(jié)目前臨床診治方法、手段及療效,為臨床治療方案的選擇提供依據(jù)與參考。為此,我們進(jìn)行了如下探討： 第一部分：外傷性視神經(jīng)病變的臨床分析研究 評(píng)價(jià)手術(shù)治療和藥物治療外傷性視神經(jīng)病變,分析影響療效的臨床因素。研究2005年1月至2010年10月太原市中心醫(yī)院臨床診斷為外傷性視神經(jīng)病變但無影像學(xué)診斷依據(jù)的患者的臨床資料。86例患者根據(jù)視力情況不同,分為A、B兩個(gè)級(jí)別組,每組分為單純藥物治療組和聯(lián)合手術(shù)治療組。將視力分為無光感、有光感、眼前手動(dòng)、眼前手動(dòng)指數(shù)和能見標(biāo)準(zhǔn)視力表(0.02以上)5個(gè)級(jí)別。對(duì)患者進(jìn)行隨訪3月,與入院視力進(jìn)行比較,視力提高1個(gè)級(jí)別者為有效,提高兩個(gè)級(jí)別及以上者為顯著,視力無進(jìn)步或者下降者為無效,觀察視力恢復(fù)情況。 得出以下結(jié)果： 1、傷后無光感患者中,藥物組與聯(lián)合手術(shù)組比較,兩者之間差別有統(tǒng)計(jì)學(xué)意義(p=0.040),聯(lián)合手術(shù)療效優(yōu)于藥物治療。 2、傷后有光感患者中,藥物組與聯(lián)合手術(shù)組比較,兩者之間差別有統(tǒng)計(jì)學(xué)意義(p=0.030),聯(lián)合手術(shù)療效優(yōu)于藥物治療。 3、接受手術(shù)患者中,傷后7天以內(nèi)手術(shù)組與7天以后手術(shù)組比較,兩者之間差別有統(tǒng)計(jì)學(xué)意義(p=0.029),7天以內(nèi)手術(shù)組優(yōu)于7天以后手術(shù)組。 由此,得出結(jié)論： 1、無論外傷性視神經(jīng)病變患者傷后有無光感,聯(lián)合手術(shù)治療的療效均優(yōu)于單純藥物治療。 2、手術(shù)時(shí)間以傷后7天以內(nèi)為佳,但即使受傷時(shí)間較長(zhǎng),也不應(yīng)輕易放棄。 3、傷后無光感、有昏迷史是影響眼視力預(yù)后的危險(xiǎn)因素,手術(shù)治療是保護(hù)視力的有力措施。 第二部分：外傷性視神經(jīng)病變動(dòng)物模型的建立與視神經(jīng)病理生理學(xué)觀察 建立接近臨床狀態(tài)的TON動(dòng)物模型,研究視神經(jīng)損傷的力學(xué)原理、神經(jīng)病理生理學(xué)改變,為臨床診療提供理論依據(jù)。 鼠頭解剖,觀察眼眶、顱底與視神經(jīng)關(guān)系。以大鼠為研究對(duì)象,對(duì)崔志利等設(shè)計(jì)的視神經(jīng)損傷方法進(jìn)行重復(fù)并改進(jìn),用小號(hào)動(dòng)脈阻血鑷夾傷視神經(jīng),建立與臨床較為接近的輕、重TON動(dòng)物模型,觀察致傷后瞳孔和直接對(duì)光反射,并行模式翻轉(zhuǎn)視覺誘發(fā)電位檢查,對(duì)正常和損傷視神經(jīng)進(jìn)行病理形態(tài)學(xué)觀察。 得出結(jié)果： 1、麻醉清醒后,所有致傷眼均表現(xiàn)為瞳孔散大、直接對(duì)光反射遲鈍或消失。無腦挫傷、感染、眶壁骨折、意外死亡 2、模式翻轉(zhuǎn)視覺誘發(fā)電位(PR-VEP)檢查：A組輕度損傷后P波潛伏期延遲,波幅降低,幅值在正常值的50%以上。B組重度損傷后波形迅速變寬平,1d時(shí)P波幅值低于正常值的50%,7d后PR-VEP不能被引出,表現(xiàn)為波形失去應(yīng)有形態(tài),無規(guī)律,波幅低,有的甚至完全消失,接近水平,即“熄滅”狀態(tài)。 3、病理學(xué)觀察：對(duì)照眼：視神經(jīng)纖維平行排列,緊密整齊,其間少量少突膠質(zhì)細(xì)胞。損傷眼：傷后1d,視神經(jīng)水腫,散在空泡樣變,血管周圍稍有滲出,未見明顯少突膠質(zhì)細(xì)胞(OLs)增生。傷后7d,空泡變性嚴(yán)重,OLs增生明顯。傷后2周,視神經(jīng)腫脹減輕,軸突分布稀疏,膠質(zhì)細(xì)胞、神經(jīng)間質(zhì)纖維組織及厚壁小血管增生。傷后4周,視神經(jīng)脫髓鞘變性嚴(yán)重,軸突裸露,大量增生的膠質(zhì)細(xì)胞以及膠原組織形成膠質(zhì)疲痕,神經(jīng)直徑縮小。B組表現(xiàn)較A組嚴(yán)重。 分析結(jié)果,得出結(jié)論： 1、本實(shí)驗(yàn)成功建立了外傷性視神經(jīng)病的動(dòng)物模型,為進(jìn)一步系統(tǒng)研究TON的機(jī)制,并為臨床上視神經(jīng)損傷患者的臨床分型、確定治療方案及預(yù)后評(píng)估提供理論依據(jù)。 2、視神經(jīng)損傷后依次經(jīng)過水腫、膠質(zhì)細(xì)胞增生和萎縮三個(gè)階段,水腫期即7d以內(nèi)治療效果好。 3、輕度損傷組傷后視神經(jīng)病理形態(tài)學(xué)改變隨時(shí)間推移損傷進(jìn)行性加重,但視神經(jīng)有一定傳導(dǎo)功能;重度損傷組傷后視神經(jīng)迅速出現(xiàn)不可逆性潰變,視神經(jīng)傳導(dǎo)功能迅速喪失。 4、PR-VEP與視神經(jīng)的病理形態(tài)學(xué)改變有很好的相關(guān)性,可以作為臨床治療的指導(dǎo)。 第三部分結(jié)論 本研究在理論和臨床實(shí)踐的基礎(chǔ)上對(duì)外傷性視神經(jīng)病變的相關(guān)問題展開研究,相關(guān)的研究結(jié)論如下： (1)本研究在理論模型的基礎(chǔ)上構(gòu)造了適合本研究的外傷性視神經(jīng)病的動(dòng)物模型,并對(duì)模型進(jìn)行了相關(guān)的理論與臨床論證,通過相應(yīng)的臨床數(shù)據(jù)分析,形成了自身的研究體系,為后續(xù)研究打下了一定理論基礎(chǔ)。 (2)無論外傷性視神經(jīng)病變患者傷后有無光感,聯(lián)合手術(shù)治療的療效均優(yōu)于單純藥物治療。 (3)在臨床中,患者受傷時(shí)間直接影響最終的治療效果,病患一周內(nèi)接受治療相對(duì)能取得臨床主動(dòng)性。 (4)視神經(jīng)損傷后依次經(jīng)過水腫、膠質(zhì)細(xì)胞增生和萎縮三個(gè)階段,水腫期即7d以內(nèi)治療效果好。 (5)視神經(jīng)和PR-VEP的相關(guān)性可以作為臨床病患診治的指導(dǎo)理論,因?yàn)閮烧咧g病變相關(guān)性較好。 (6)輕度損傷組傷后視神經(jīng)病理形態(tài)學(xué)改變隨時(shí)間推移損傷進(jìn)行性加重,但視神經(jīng)有一定傳導(dǎo)功能;重度損傷組傷后視神經(jīng)迅速出現(xiàn)不可逆性潰變,視神經(jīng)傳導(dǎo)功能迅速喪失。
[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.
【學(xué)位授予單位】：山西醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2011
【分類號(hào)】：R779.1

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