This Article  • References  • Full text PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citing articles on HighWire  • Citing articles on Web of Science (11)  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

Thomas C. Spoor, MD; John G. McHenry, MD; Dong H. Shin, MD, PhD
Detroit, Mich

Arch Ophthalmol. 1994;112(1):25-26.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 . . . [Full Text PDF of this Article]

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?