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Traumatic optic neuropathy (traumatic optic neuropathy, TON) is the most common type of optic nerve damage, and its blunt head trauma accounts for about 0.5% to 5%, after injury, severe visual impairment, poor prognosis, approximately 50% of patients remaining permanent loss of vision. Clinical findings in some patients can recover without treatment, some patients have no signs of recovery any treatment, and some patients to take timely and effective treatment can often achieve good results. Currently dominated glucocorticoid drug therapy and surgical therapy is commonly used treatment, endoscopic optic nerve decompression surgery has become the main method of treatment. However, different scholars reported that the surgery also vary widely. In order to fundamentally understand traumatic optic neuropathy in the pathogenesis, to better guide the clinical diagnosis and treatment, we carried out the following studies: Part I: traumatic optic neuropathy clinical analysis of surgical and conservative treatment TON evaluate the efficacy, impact analysis A clinical factors. For 95 cases (100) were diagnosed TON retrospective analysis of clinical data, row endoscopic optic canal decompression therapy 47 cases (48) classified as surgical group, 48 cases of drug therapy alone (52), in the final conservative groups. Will be divided into light perception vision, light perception, hand movement, the immediate index and visibility standard vision chart (0.02 or more) five levels, namely counted as Ⅰ ~ Ⅴ grade. Up 3 to 12 months, visual acuity recovery. By observing the following results: 1. Surgery group confirmed by surgery 40 (40/48) of the optic canal fracture, CT diagnosis of 23 fractures, CT was 57.5% of diagnosed (23/40). 2 hospitalized vision surgery group Ⅱ ~ Ⅳ grade of eyes was significantly better than the conservative group. 3 hospitalized suffering from eye sight Ⅰ level, the impact of hormone therapy improved vision after surgery than those who did not change. 4 surgery group and conservative group, admission acuity grade Ⅱ ~ Ⅳ was significantly better than suffering from eye sight admission grade Ⅰ. 5. Surgery group and conservative group, vision grade Ⅱ ~ Ⅳ suffering from eye injuries to persons within the treatment time in 7d 7d more effective than those. Thus, the conclusion: 1. Imaging optic canal without fracture, surgery should not be the determining factor whether. (2) more than light perception before surgery, surgical therapy is superior to medical therapy alone. 3 admission no light perception and high-dose corticosteroid therapy without improvement, the prognosis is poor, unless the patient is urged to discard surgery; has improved by surgery better. 4 hospitalized light perception and light perception vision more, high-dose corticosteroid treatment, visual acuity improved significantly if the two level and above who can be treated conservatively; such as a slight increase, should be treated surgically, compared with postoperative results good. 5 length of the course is an important factor affecting the efficacy, the need for early treatment, and surgery should be performed within the 7d. Part II: experimental traumatic optic neuropathy animal model of optic nerve pathophysiology establish close clinical observation status TON animal model to study the mechanics of optic nerve damage, nerve pathophysiology, provide a theoretical basis for clinical diagnosis and treatment. Tutou Anatomy: observation orbit, skull base and optic nerve relationship. In New Zealand white rabbits as the research object, the king first-class design repeat optic nerve damage and improved methods, the application of a spring gun given instant impact force, the establishment of closer and clinical light and heavy TON animal model, the two kinds of damage general quantitative intensity of injury observed after injury and direct pupil light reflex, parallel mode reversal visual evoked potential for damage to the optic nerve of normal and pathological morphology. Through observation, the following results: 1. Awake after anesthesia, all eye injuries are expressed as mydriasis, direct light reflex slow or disappear. No brain contusion, infection, orbital fracture, accidental death. One case of optic nerve sheath fault but incomplete. 2 mode reversal visual evoked potentials modeling latency and amplitude of P wave front left and right eye, the difference was not statistically significant (p> 0.05). A group of P-wave latency after mild injury delay, amplitude decreased 1 d after injury in the normal amplitude of more than 50%; B group of severe injury level waveform widens rapidly after injury 1 dP amplitude is below normal 50%, 7d when the PR-VEP could not be elicited. Each time point compared with the control group, the difference was statistically significant. 3 pathological morphology control eye: optic nerve fibers arranged in parallel, closely arranged, during which a small amount of oligodendrocytes. Eye injury: injury 1d, optic nerve edema, scattered vacuolar degeneration, perivascular slight exudation, no significant oligodendrocytes (OLs) hyperplasia. 1 week after injury, degeneration serious, OLs marked hyperplasia. 2 weeks after injury, optic nerve swelling reduced axon sparse, glial cells, nerve tissue and thick fibrous stromal proliferation of small blood vessels. 4 weeks after injury, severe degeneration of the optic nerve demyelination, axonal exposed, a large proliferation of glial cells and glial scar tissue formation of collagen, reduced diameter nerves. Group B than in group A serious performance. Analytical results obtained: 1 This experiment successfully established traumatic optic neuropathy animal model for further systematic study TON mechanisms for clinical optic nerve damage in patients with clinical classification, determine treatment options and prognosis provide a theoretical basis . 2 turn after optic nerve injury edema, gliosis and atrophy in three stages, namely 7d edema within therapeutic effect. 3 mild group pathological changes in the optic nerve after injury over time damage progressively increased, but there is a certain nerve conduction; severe injury occurs rapidly after injury irreversible optic nerve degeneration, optic nerve conduction rapid loss. 4.PR-VEP and pathological changes in the optic nerve has a good correlation can be used as clinical treatment guidance. But higher than normal for the amplitude decreased to 50% of patients to regulate timely treatment, should have access to good effect.
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