Optic nerve sheath decompression is an effective treatment for pseudotumor cerebri and visual loss. Although this treatment is successful in reducing papilledema and improving visual function in 80% to 90% of patients, 30% of successful optic nerve sheath decompressions eventually fail.1 There are several treatment options after a failed optic nerve sheath decompression: repeated optic nerve sheath decompression, acetazolamide sodium, lumboperitoneal shunting, serial lumbar punctures, and corticosteroids. Acetazolamide use is limited by patient intolerance, gastrointestinal-tract side effects, and paresthesia. Corticosteroids are only practical in the short term and can increase intracranial pressure when therapy is tapered. Lumboperitoneal shunts frequently fail and become infected, and visual loss may continue in spite of a functioning shunt. Repeated optic nerve sheath decompressions require meticulous dissection through extensive orbital scarring and are not as successful as primary decompressions.1
Controversy exists as to the mechanism of action of optic nerve sheath decompression. We
Spoor TC, McHenry JG, Shin DH. Optic Nerve Sheath Decompression With Adjunctive Mitomycin and Molteno Device Implantation. Arch Ophthalmol. 1994;112(1):25–26. doi:10.1001/archopht.1994.01090130035009
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