I have seen too many patients with intracranial hypertension compressive optic neuropathy who come to me too late for consultation, and I cannot blame the local doctors for this, as the treatment of this disease is so backward in this country. I have been making appeals since I returned to China, but the impact has been minimal. I hope that through this platform, more doctors (neurologists, surgeons, ophthalmologists) can understand the diagnosis and treatment of this disease, and help more patients to get early treatment and recovery. Intracranial hypertension is a condition in which intracranial pressure is elevated and sustained above 2.0 kPa ( 15 mmHg, 200 mm water column) due to excessive secretion of fluid from the dorsum of the brain, impaired absorption, obstruction of circulation, or swelling of the brain tissues, intracranial space-occupying lesions, or excessive cerebral blood flow perfusion. Because the optic nerve sheath is continuous with the intracranial dura mater and arachnoid, the high intracranial pressure is transmitted to the ophthalmic end of the optic nerve through the sub optic nerve sheath gap; the optic nerve sheath forms a cuff-like blind tube around the optic nerve at the proximal orbital end of the optic nerve, and the intracranial pressure is transmitted to the end of the blind tube to produce a higher compressive force, leading to optic papillary ischemia, hypoxia, and bilateral (and unilateral) optic papillar edema within a few hours to several days to form an intracranial hypertensive optic papillae (IPOP). Intracranial hypertensive optic papilloedema. Funduscopic examination of the patient shows bilateral bulging of the optic papillae with blurred borders, loss of optic papillary vein pulsation, tortuous dilatation of the veins, and may be accompanied by superficial hemorrhage. In the early stage, there are no obvious symptoms; with the progress of the disease, transient blurring of vision, abnormal color vision, or transient loss of vision, usually lasting only a few seconds, but a few can be up to about 30 seconds; mild visual acuity loss (0.8 or so) or darkening of the error, contrast loss is often seen in intracranial hypertension lasts for 1 to 2 months, and the visual field can be physiologically blinded to enlargement; if the high intracranial pressure continues to persist, the visual field will be narrowed to varying degrees, and the visual field will be reduced. then varying degrees of narrowing, further deterioration of visual acuity, decline; 3-6 months later, the patient’s visual acuity declines rapidly, the field of vision is rapidly narrowed, often at 0.1 or below; advanced due to intracranial hypertension and optic nerve sheath high pressure can not be effectively relieved, resulting in irreversible permanent loss of vision, blindness or light-sensitive vision. Common intracranial hypertensive disorders include: meningitis of various causes (cryptococcal meningitis, purulent meningitis, syphilitic meningitis, tuberculous meningitis); intracranial venous sinus thrombosis of various causes; idiopathic intracranial hypertension (benign intracranial hypertension); and intracranial hypertension secondary to intracranial occupations such as tumors.