S S is a 47 year old professor from a local university who was sent for cataract evaluation. The patient complains of impaired vision at all distances for the past several months. Additionally, he reports that his visual dysfunction has progressed over the course of the past year, especially with reading and fine detail work. The patient’s past ophthalmic history and medical history are negative. He denies any history of tobacco as well as illicit drug use, the patient does claim that he has an “occasional” drink. He takes no medications and has no known medical allergies.

On examination, the BCSA is 20/200 OD and 20/80 OS. The patient’s refraction is OD -2.50-2.25x005, and OS is -1.25-1.50x160. There is no improvement with pinhole occlusion. Pupils are reactive without a relative afferent pupillary defect. Confrontation fields are unremarkable, but the patient’s responses are inconsistent, presumably on the basis of decreased vision OD. Extraocular motions are smooth, accurate, full and extensive.

Intraocular pressures by applanation tonometry are 13mm Hg OU, and kerotometry mires are sharp, and consistent with the patient’s refraction.

Slit lamp examination finds the adnexa to be benign. The conjunctivae are white and quiet and the patient’s corneas are clear and compact. The crystalline lenses demonstrate symmetric trace posterior subcapsular cataracts. The remainder of the anterior segment examination is within normal limits.

Dilated fundoscopy is also within normal limits bilaterally, with sharp, well-perfused discs and a cup-to-disc ratio of 0.4 OU.

Assessment/Plan

This case presents a few inconsistencies. The patient appears to be a reliable historian, yet relates progressive visual difficulty in the setting of only trace cataracts. Furthermore, there is no improvement with pinhole occlusion or refraction. Additionally, while there were cataracts evident in each eye, the clinical appearance of these changes was symmetric, and therefore did not support the relative disparity in acuity noted between the two eyes.

Due to the apparent inconsistency between physical signs and symptoms, a work-up for unexplained vision loss was initiated. The first test performed was a Humphrey 30-2 visual field. 

Humphrey visual field analysis manifests a relative bitemporal hemianopia, and suggests a compressive lesion of the optic chiasm. Accordingly, an MRI of the optic chiasm was obtained and demonstrated the following:

This MRI demonstrates a large sellar mass with supracellar extension. The sella (the floor of the cranial vault where the pituitary gland typically resides) is expanded. No normal pituitary gland is noted. There appears to be extension into the cavernous sinuses. The mass measured approximately 2.7 x 2.1 x 2.0cm! The lesion appearance on MRI was consistent with a macroadenoma of the pituitary gland. Accordingly, neurosurgical consultation was obtained and the patient underwent resection of the lesion.

Discussion:

Neurons from each optic nerve cross or decussate at the optic chiasm. Lesions that are anterior to the chiasm characteristically result in monocular vision loss and also cause a relative afferent pupillary defect (Marcus-Gunn Pupil). One will note different patterns of bitemporal field loss, and (as in this case) asymmetric field defects are not uncommon.

Parasellar lesions characteristically result in bilateral progressive visual loss. The findings of chiasmal lesions are protean – the nerves may appear normal, as in our patient or atrophic. More commonly, the nerves manifest a focal temporal atrophy, related to neuron loss from the papillomacular bundle. Another manifestation of a chiasmal lesion is increased cupping – hence the rational for imaging in patients presumed to have” low tension” glaucoma.

Happily, our patient has done well following the resection of his tumor. My thanks to his optometrist for keeping this anterior segment surgeon on his toes!