Treatment of cryptococcal meningitis secondary to intracranial hypertensive compression optic neuropathy: Optic nerve sheath dissection and decompression, causes of vision loss in patients with cryptococcal meningitis: 1. Patients with acute high cranial pressure compressing the optic nerve, resulting in bilateral optic papillary edema, rapid loss of vision, and blurred vision; if cranial hypertension persists or is progressively elevated and is not effectively controlled or relieved for a long time, it will compress the optic nerve for a long time and This will further lead to narrowing of the visual field and eventual blindness. 2, a small number of patients (position) of the auditory nerve, facial nerve, abducent cerebral nerve by continuous intracranial hypertension compression appears partial or complete paralysis, hearing loss, double eye abduction restrictions, etc.. Although the pathology report (or autopsy) shows that the main pathology of patients with cryptococcal meningitis is in the meninges and brain pools, (largely showing meningeal vascular congestion, widening of the brain gyrus, shallowing of the brain sulcus and clouding of the soft meninges, especially at the base of the brain. Yellow sticky jelly-like exudate can be seen in the pontine pool, optic chiasm, cerebellar medullary pool, lateral sulcus, base of the brain and dilated subarachnoid space.) However, in a small number of patients, small granular nodules or sacs with gelatinous exudates were seen in the brain tissue; damage to the brain parenchyma by cryptococci could not be excluded. In a small number of cases, after optic nerve sheath dissection and decompression, a biopsy of the optic nerve sheath showed the presence of Cryptococcus in the optic nerve sheath, suggesting that Cryptococcus itself may attack the optic nerve, i.e., it is possible that Cryptococcus or its toxin itself was involved in the damage to the optic nerve. The procedure and principles of optic nerve sheath dissection and decompression optic nerve sheath dissection and decompression is a direct transorbital procedure that exposes the intraorbital segment of the optic nerve and dissects the intraorbital segment of the optic nerve sheath to drain the cerebrospinal fluid into the orbital tissue and reduce intracranial pressure. The blind end of the optic nerve sheath at the optic papilla is preferred, resulting in a much higher pressure on the optic nerve than on the rest of the optic nerve. With this procedure, the pressure and compression at the blind end of the optic papilla of the optic nerve sheath is effectively relieved. The clinical manifestations are: disappearance of optic papillary edema, improvement of visual acuity, decrease of intracranial pressure, and reduction or disappearance of meningeal irritation signs. This procedure is currently used abroad mainly in patients with decreased visual acuity due to benign intracranial hypertension (aka: idiopathic intracranial hypertension, cerebral pseudotumor, IIH), and post-traumatic subarachnoid hemorrhage of the optic nerve (our report of successful surgery will be mentioned later), and may be useful in non-arteritic ischemic optic neuropathy patients. In fact, optic nerve sheath dissection and decompression is the best option for any cause of vision loss due to increased intracranial pressure and thus compression of the optic nerve, or visual field defects or narrowing. This procedure is superior to optic nerve canal decompression in terms of complexity and risk control, and is no less effective than optic nerve canal decompression.