Basic knowledge about optic nerve injury A. Concept Clinically, optic nerve injury is called traumatic optic neuropathy, which is one of the common and serious complications of craniocerebral injury, accounting for about 2% to 5% of craniocerebral trauma. According to the cause of injury, it is divided into car accident injury, fall injury and blow injury, among which the most common one is car accident injury. Due to the anatomical structure and physiological characteristics, more than 90% of optic nerve injuries are indirect injuries to the optic nerve canal segment. Direct injuries caused by sharp objects piercing the optic nerve and direct injuries to other parts of the optic nerve are relatively rare in clinical practice. Indirect optic nerve injury refers to the impact on the lateral aspect of the orbit, usually the upper temporal part of the brow arch, and the external force is transmitted to the optic nerve canal through the skull, causing deformation or fracture of the optic nerve canal, resulting in optic nerve injury and causing visual acuity and visual field impairment. Second, the diagnosis of post-traumatic vision loss, visual field defects and abnormal afferent pupillary reflex to light is the main clinical basis for the diagnosis of optic nerve injury. Comprehensive diagnostic criteria: ① history of head trauma; ② visual impairment; ③ pupil dilatation on the side of injury, loss of direct light response, presence of indirect light response; ④ fundus examination is normal in the early stage, but optic nerve atrophy can be seen in the late stage; ⑤ visual field defects appear in those with incomplete loss of vision, and the lower half of the visual field defects are most common; ⑥ CT or MR scan reveals optic nerve canal fracture, peri-optic nerve hematoma compression or optic nerve edema; electrophysiology Flash visua evoked potential (FVEP) examination with loss of P100 wave amplitude or prolonged latency. A dilated pupil on the affected side, a blunted or absent direct light reflex, and the presence of an indirect light reflex may be the only signs of optic nerve injury. During the examination, the pupil of the affected eye is observed first, and then the pupil of the healthy eye is observed; otherwise, the observation time is long and the two pupils can be the same size, which interferes with the diagnosis of optic nerve injury. The fundus may be normal in the early stage. For those who are confused, the pupil of the affected eye is dilated and the direct response to light is absent or blunted, while the indirect response to light is normal is a typical sign of optic nerve injury, but it should be differentiated from brain herniation and articulated nerve injury; for patients with combined anterior skull base fractures, bilaterally bruised and edematous eyelids or ocular bandages are easily neglected, and eyelid pulling hooks should be applied to open the lids for examination if necessary. Treatment Once this disease is diagnosed it should be treated with immediate resuscitation therapy along with the treatment of traumatic brain injury. Preferred medication, high doses of corticosteroids, energy synergists, hypertonic dehydrating agents, cytarabine, vitamin B group drugs, vasodilators can reduce tissue edema, reduce the compression of the optic nerve, prevent and treat post-injury vasoconstriction and spasm, and promote the recovery of blood circulation and optic nerve conduction function. If there is clear compression of the optic nerve canal fracture and intracanalicular hematoma on CT or X-ray, decompression and opening of the optic nerve canal should be performed as soon as possible. Because of the cranial trauma are mainly to save the cranial trauma and life, optic nerve injury can not be detected or ignored, or even have not considered this aspect of the problem, until the condition is stable this is found to have visual impairment, when the ophthalmology consultation has been days, days or more, delaying the possible effective treatment time. It has been suggested that timely decompression of optic nerve injury (within 48 h) is significantly better than late decompression (14 days); it has also been reported in the literature that there is little difference in the degree of nerve function decline between 4 days and 60 days after trauma. Therefore, it is recommended that after high-dose corticosteroids and active vasodilating and nerve-nourishing medication after optic nerve collision and crush injuries, if the visual acuity still does not recover or progressively decreases within 48 h, surgery should be performed immediately, supplemented with hyperbaric oxygen therapy. Fourth, the prognosis 1, the degree of post-injury visual impairment: post-injury light perception, indicating that the optic nerve still has neurons alive, after active treatment, the prognosis is better. The prognosis is poor because there is no light perception after the injury, which means that few neurons survive or even all of them are apoptotic. 2.The time from injury to the start of treatment: the treatment started within 7 days after the injury, its efficacy is significantly better than those who started treatment after 7 days. 3, optic nerve electrophysiological examination results: in general, the majority of VEP extinguished after the injury is no photoreceptors, especially 2 weeks after the injury VEP is still extinguished state, its vision basically can not be restored.