Steven A. Newman

A Clinicopathologic Study of Optic Neuropathies Associated by Intracranial Mass Lesions by Quantification of Remaining Axons

We examined three patients with intracranial mass lesions that damaged the anterior visual pathway and studied this damage histologically after the patients died. Estimation of the number of surviving axons in the six optic nerves generally showed the greatest atrophy to be in the temporal sector in cross sections immediately behind the globe. More posterior to the globe, atrophy appeared greatest in the center of several nerves. This pattern of damage may result from particular vulnerability of macular axons to damage along the anterior visual pathway. Optic disk pallor was present in two eyes that had less than 40% of the normal number of axons remaining, while one optic disk appeared to be normal with 70% of the axons intact. Afferent pupillary defects were observed in two patients who had two to three times as many remaining axons in the contralateral optic nerve as in the nerve on the side of the defect.

Orbital Inflammatory Disease After Intravenous Infusion of Zoledronate for Treatment of Metastatic Renal Cell Carcinoma

Town,SouthAfrica(DrC.L.Shields); Mellon Charitable Giving from the Martha W. Rogers Charitable Trust, Philadelphia, Pennsylvania (Dr C. L. Shields); the LuEsther Mertz Retina ResearchFoundation,NewYork,New York (Dr C. L. Shields); a donation from Michael, Bruce, and Ellen Ratner, New York (Drs C. L. Shields and J.A.Shields); theEyeTumorResearch Foundation, Philadelphia (Drs C. L. ShieldsandJ.A.Shields);andthePaul Kayser International Award of Merit in Retina Research, Houston, Texas (Dr J. A. Shields).

Ocular vaccinia with severe restriction of extraocular motility.

Comment. Macular edema is likely involved in FTMH pathogenesis and persistence. In our case, the macular edema reduction occurred first, presumably as a result of NSAID therapy. Closure of the macular hole followed. This implies a direct cause-and-effect relationship with NSAID treatment. Topical NSAIDS have been shown to reduce macular edema more than 24 months after cataract extraction, but persistent use is often needed. The cause of macular edema and FTMH reopening in our patient is not readily evident but may relate to an abnormality of the retinal surface. The foveal contour in one of the most recent OCT images is irregular but shows no epiretinal membrane (Figure 2C). In some patients with FTMH, histopathologic study revealed that a thin rim of cortical vitreous remains attached to the retinal surface. Unfortunately, this layer cannot be seen consistently with biomicroscopy, OCT, or ultrasonography. Although we found no other cases of FTMH closure related to topical NSAID use, we did find a case report of a patient with an FTMH and macular edema associated with HLA-B27–associated uveitis. Treatment of the macular edema with a peribulbar triamcinolone acetonide injection led to vision improvement and FTMH closure. Another study implicating macular edema in FTMH pathogenesis demonstrated an increased risk of FTMH reopening in patients undergoing cataract extraction. The risk was 7-fold higher in patients with clinically apparent cystoid macular edema. One study done prior to routine use of OCT indicated that approximately 8% of patients with FTMHs have spontaneous regression. It could be argued that the initial closure of the FTMH in our patient was spontaneous and coincided with the NSAID treatment. However, reopening when the NSAID was discontinued and reclosure when the NSAID was restarted make a strong case that the NSAID directly contributed to the closure of this FTMH. This case demonstrates a probable role for topical NSAID treatment in a patient with an FTMH.