||The patient is a 60-year-old woman with a chief complaint of decreased vision. In 1986 she was diagnosed with a poorly differentiated breast cancer in her left breast. She underwent mastectomy, and all nodes were negative. She did well until 1991, when she was found to have a chest wall mass. This mass was excised and pathology was found to be consistent with recurrent tumor. Estrogen and progesterone receptors were positive, and the patient was placed on Nolvadex (tamoxifen citrate). In the summer of 1990, the patient noted horizontal diplopia. She also felt that she had a decrease in her peripheral vision. An ophthalmologic examination at that time was felt to be unremarkable. In June 1991, she had visual fields done that showed a bitemporal hemianopia pattern. An MRI was done on June 7, 1991, which was read as ""essentially negative MRI of the head."" A few small focal areas of increased intensity deep in the white matter were noted. She underwent a neurologic examination, with no abnormalities detected except for a possible peripheral neuropathy based on pinprick, vibration, and light-touch testing. A lumbar puncture was considered, but not performed. Vitamin therapy was recommended. A B12 lever was normal. the patient was seen in neuro-ophthalmologic consultation in July 1991. Current medicines included multivitamins, quinine (for leg cramps), Robaxin, and Nolvadex. There was a distant history of alcohol abuse. the patient also noted headaches every few days that were relieved by Tylenol. She apparently had lost about 30 pounds over the last few months. Vision was 6/200 OD and 8/200 OS. Motility was full, with normal saccades, pursuit, and optokinetic nystagmus responses. Large central scotomas were noted by confrontation, and nasally preserved fields only OU were noted by Goldmann. There was no APD, but pupils were very sluggish OU. Fundi showed possible slight temporal pallor OU. Postfixation blindness was present, consistent with severe bitemporal hemianopia. Her original MRI was reviewed and was believed to show an abnormal position of the chiasm. It appeared that the chiasm was being elevated superiorly by an isodense mass. Repeat MRI with attention to this region confirmed the impression of a suprasellar arachnoid cyst. Baseline endocrine studies demonstrated borderline low-thyroid tests. She underwent neurosurgery on July 31, 1991, her vision had returned to 20/30 OU and her Goldmann fields were full. Mild optic nerve pallor was present. Arachnoid cysts are collections of CSF contained within a leptomeningeal lined cavity. They can be found at any location adjacent to the subarachnoid space. Most of these lesions are felt to be developmental. They may also result from trauma, inflammation, or infection. Occasionally, they may be associated with an adjacent tumor. Most are located in the middle cranial fossa. Suprasellar arachnoid cysts occur infrequently with only 13.5% of these occurring in patients over 20 years old. There may be associated hydrocephalus. One possible treatment is to incise and drain the cyst and allow it to communicate with the ventricular system or subarachnoid space.