More and more patients are coming to me for optic papilledema, vision loss, empty butterfly saddle, tinnitus, etc. I regret that they are coming too late, and I regret that many doctors are still using outdated knowledge from 20 or 30 years ago to guide the diagnosis and treatment of this group of patients. I hope that with my articles more patients will receive timely and effective treatment. Optic nerve papilledema, is a non-inflammatory obstructive edema of the optic papilla. Most of them are caused by systemic diseases, and the most common and major cause is increased intracranial pressure; such as intracranial occupying lesions (brain tumor, brain hemorrhage, brain abscess, brain parasitosis, etc.), increased cerebrospinal fluid or obstruction of cerebrospinal fluid reflux during intracranial inflammation (various meningitis: tuberculosis, cryptococcal, etc.) (various intracranial venous sinus thrombosis, etc.), traumatic brain injury, abnormal brain development, hydrocephalus, cerebral edema, etc. It can also be caused by perforated eye injury, low eye pressure formed by corneal fistula, and obstruction of hemolymphatic return caused by intraorbital tumor or hematoma. Clinical manifestations of patients: 1. Initial stage of edema: There are often paroxysmal transient visual hooding (i.e.: seeing clearly for a while; blurring for a while, especially blurred vision is obvious after bending), but the visual acuity table vision can be completely normal. Afterwards, as the disease progresses, episodes of transient visual blindness become more frequent, and even transient blackness occurs (this happens when the patient stands up quickly or turns his head sharply, so he moves slowly and cautiously), and his visual acuity begins to gradually decrease, but the strength is mildly impaired, probably between 0.6 and 0.8. Visual field examination reveals an enlarged physiological blind spot. If the papilledema cannot be relieved for a long time, the optic nerve fibers will be progressively atrophied and the visual impairment will become more and more severe, and the visual field will have centripetal narrowing in addition to the physiological blind spot enlargement. Since the majority of patients with bilateral optic nerve papilledema are caused by intracranial occupying lesions, intracranial venous sinus thrombosis, or increased intracranial pressure due to systemic diseases, patients may present with headache, nausea, vomiting, and other related signs and symptoms. Early changes in the fundus: papillary congestion, unclear boundary between the nasal side and the upper and lower sides, and shallow physiological depression. 2. Increased edema: rapid decrease in visual acuity, progressive narrowing of the visual field, some patients’ vision decreases to manual or light perception in front of the eyes. It is often accompanied by headache, dizziness, tinnitus, decreased thinking, and neck pain. 3. Fundus examination: The various fundus changes mentioned above are becoming more and more obvious. The papillary edema and congestion gradually increase and expand in all directions, making the boundary more blurred or even disappear completely; the papillae are generally higher than 3.0D out of the retinal plane, and in severe cases, they can exceed 7.0D; the retinal veins become angry and tortuous, and the ratio of arteriovenous diameter is from 1:2, 1:3, or even more than 1:4; the surface of the edematous papillae and their surroundings can be seen as linear or flame-like hemorrhagic spots, with varying numbers and sizes. The degree of edema is not necessarily proportional to the height of intracranial pressure, and seems to be more closely related to the location of intracranial occupying lesions. Head CT or MRI manifestation: empty sella syndrome (empty sella syndrome, due to septal defect or pituitary atrophy, the subarachnoid space protrudes into the saddle under the impact of cerebrospinal fluid pressure, resulting in the enlargement of the saddle); chronic intracranial pressure increase causes the most likely vacuolated saddle. At present, CT and MRI are reliable methods to diagnose vacuolated saddle syndrome, especially MRI has the highest diagnostic accuracy, which can clearly show the thinning of the pituitary gland under pressure and posterior displacement, mainly manifested as follows: (1) The saddle is enlarged or normal, and the saddle is filled with a large amount of cerebrospinal fluid, showing obvious long T1 and long T2 signals. (2) The pituitary gland is compressed and flattened, with a thickness of ≤3 mm, and is in a short arc in the sagittal position, and in the coronal position, the pituitary stalk is centered in the coronal position, and its posterior displacement is visible in the sagittal position.