Ther Adv Neurol Disord. 2016 Sep;9(5):436-40. doi: 10.1177/1756285616655264. Epub 2016 Aug 15.
Martinez-Lapiscina EH1, Sepulveda M1, Torres-Torres R2, Alba-Arbalat S1, Llufriu S1, Blanco Y1, Guerrero-Zamora AM1, Sola-Valls N1, Ortiz-Perez S2, Villoslada P1, Sanchez-Dalmau B2, Saiz A1.
Neuromyelitis optica spectrum disorder (NMOSD) is an inflammatory central nervous system disease that preferentially affects the optic nerve and spinal cord [Wingerchuk et al. 2015]. Up to 70% of patients with NMOSD have antibodies to aquaporin-4 (AQP4-IgG). AQP4 is expressed in astrocytes of the optic nerve and Müller cells in the eye. A subgroup of AQP4-IgG-seronegative patients has antibodies to myelin oligodendrocyte glycoprotein (MOG-IgG), and optic neuritis (ON) relapses are also frequent in these patients [Höftberger et al. 2015].
We hypothesize that retinal injury may be additionally driven by Müller cells dysfunction in patients with AQP4-IgG. This condition, in contrast with those patients who harbour MOG-IgG, may induce differential changes in the outer retinal layers. In this brief series of cases, we aim to investigate if optical coherence tomography (OCT) may distinguish ON associated with AQP4-IgG or MOG-IgG in NMOSD.