Pituitary adenomas account for at least 12% of all intracranial neoplasms1. Their incidence is estimated to be 20 to 30 per million2. Approximately 25% to 30% of patients with pituitary adenomas do not have a classic hypersecretory syndrome such as acromegaly, Cushing disease, or prolactinoma. Tumors that do not appear to secrete hormones are called nonfunctioning adenomas (NFA)3. NFAs often present with signs of mass effect, such as visual changes, and symptoms of pituitary insufficiency4.
Radiation therapy plays an important role in the treatment of NFAs. In the past, radiation therapy alone was the treatment of choice unless there were large visual deficits, in which case a craniotomy was performed to decompress the optic nerves and
chiasm. With improving microsurgical techniques, the preferred treatment became neurosurgery followed by radiation therapy for extensive bulky lesions, histologically invasive adenomas, or incomplete excision5. The routine use of post-operative radiation therapy in case of residual tumor is controversial6-9; its use prevents regrowth of residual tumor in most cases, but it may cause such side effects as radiation optic neuropathy (RON)10,11. The incidence of RON after external beam radiation therapy for NFA has not been well-documented. There is also debate as to whether patients with NFA are less likely to have RON development after radiation therapy than those with growth hormone-secreting or adrenocorticotropic hormone-secreting pituitary adenoma12-17.
The aim of this retrospective study was to discover the incidence of RON in a cohort of irradiated patients with NFA. Also, a review of prior published series and individual case reports is presented, from which an estimation of the incidence of RON in irradiated NFA can be deduced.