Purchase this article with an account.
F. X. Venzara, III, L. M. Ventura, V. Porciatti; Reversible Dysfunction of Retinal Ganglion Cells in Compressive and Non-Compressive Pituitary Tumors. Invest. Ophthalmol. Vis. Sci. 2007;48(13):928.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
To evaluate the impact of a mass lesion at the optic chiasm on retinal ganglion cell (RGC) function.
Three patients with increased cupping of the optic nerve, but normal visual acuity (VA) and intraocular pressures (IOP), were participating in a longitudinal study monitoring for glaucoma progression that included serial pattern electroretinogram (PERGLA paradigm, Porciatti and Ventura, Ophthalmology 2004), standard automated perimetry (SAP), and Optical Coherence Tomography (Stratus OCT: program RNFL fast scan) measurements. Excessive PERG deterioration during the follow up period prompted additional testing to include MRI imaging of the brain. In all three patients, MRI revealed a pituitary tumor, one of whom showed no evidence of chiasmal compression. All tumors were non-secreting, and were removed according to standard procedures.
During the follow up period there were no changes in VA or IOP, but SAP showed bitemporal changes pre-operatively in one of the patients with chiasmal compression. In contrast, during the pre-surgical period, six eyes of three patients displayed progressive PERG dysfunction. PERG showed an average reduction of amplitude of 42.5% [SD 7.6] and an average phase delay of 4.4% [SD 4.4]. Following tumor resection, the PERG amplitudes progressively recovered to normal values.
Results indicate that pituitary tumors may cause RGC dysfunction, even in the absence of direct mechanical compression of the optic chiasm. Such dysfunction may be reversed by tumor reduction. Reversible RGC dysfunction may occur in chiasmal compression through blockage of retrograde axonal transport of neurotrophins. In non-compressive conditions, dysfunction may be linked to interference in axonal flow induced by local ischemia at the level of the optic chiasm (Cioffi, Trans Am Ophthalmol Soc 2005). A potential candidate for this hemodynamic perturbation is the potent vasoactive peptide endothelin-1 released by the pituitary tumor (Lange et al, J Clin Endocrinol Metab 1994).
This PDF is available to Subscribers Only