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BARCELONA—In addition to its neuroprotective effect on the peripapillary retinal nerve fiber layer, sodium channel blockade with phenytoin also appears to prevent degeneration of the macular ganglion cell complex after acute optic neuritis, according to data presented at the 31st Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS).
Rhian E. Raftopoulos, MbChb, of University College London, and colleagues previously reported in a phase II trial that sodium channel blockade with phenytoin is neuroprotective in acute optic neuritis. The primary outcome measurements were the thickness of the peripapillary retinal nerve fiber layer and macular volume, measured using optical coherence tomography (OCT).
In the present study, the researchers sought to determine whether this neuroprotective effect is selective for particular anatomical layers of the retina. They enrolled patients with acute optic neuritis and randomized them within two weeks of symptom onset to receive phenytoin or placebo for three months. Spectral domain fast macular and papillomacular bundle (PMB) OCT scans were performed at baseline and after six months. Masked automated retinal layer segmentation was performed to obtain average thickness measures of retinal nerve fiber layer, ganglion cell and inner plexiform layer (GC/IPL), and the composite ganglion cell complex. The ganglion cell complex (GCC) encompassed the retinal nerve fiber layer plus GC/IPL. Active versus placebo differences in mean six-month affected eye retinal nerve fiber layer, GC/IPL, and GCC were calculated from macular (n=60) and PMB (n=48) scans, adjusted for the corresponding baseline measurements in the unaffected eye.
At baseline, the mean thicknesses of the retinal nerve fiber layer, GC/IPL, and GCC were similar in the active and placebo groups in the macula and papillomacular bundle. In the intention to treat comparison, mean adjusted affected eye macular retinal nerve fiber layer thickness at six months was 4.67 μm greater in the active group (a 42% treatment effect). Mean adjusted macular GCC thickness was 5.63 μm greater in the active group (a 28% treatment effect). Treatment had no significant effect on macular GC/IPL when measured alone.
In the papillomacular bundle, mean adjusted retinal nerve fiber layer thickness was 2.49 μm greater in the active group at six months, mean GC/IPL thickness 2.79 μm greater, and mean GCC thickness 5.41 μm greater.
BARCELONA—In addition to its neuroprotective effect on the peripapillary retinal nerve fiber layer, sodium channel blockade with phenytoin also appears to prevent degeneration of the macular ganglion cell complex after acute optic neuritis, according to data presented at the 31st Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS).
Rhian E. Raftopoulos, MbChb, of University College London, and colleagues previously reported in a phase II trial that sodium channel blockade with phenytoin is neuroprotective in acute optic neuritis. The primary outcome measurements were the thickness of the peripapillary retinal nerve fiber layer and macular volume, measured using optical coherence tomography (OCT).
In the present study, the researchers sought to determine whether this neuroprotective effect is selective for particular anatomical layers of the retina. They enrolled patients with acute optic neuritis and randomized them within two weeks of symptom onset to receive phenytoin or placebo for three months. Spectral domain fast macular and papillomacular bundle (PMB) OCT scans were performed at baseline and after six months. Masked automated retinal layer segmentation was performed to obtain average thickness measures of retinal nerve fiber layer, ganglion cell and inner plexiform layer (GC/IPL), and the composite ganglion cell complex. The ganglion cell complex (GCC) encompassed the retinal nerve fiber layer plus GC/IPL. Active versus placebo differences in mean six-month affected eye retinal nerve fiber layer, GC/IPL, and GCC were calculated from macular (n=60) and PMB (n=48) scans, adjusted for the corresponding baseline measurements in the unaffected eye.
At baseline, the mean thicknesses of the retinal nerve fiber layer, GC/IPL, and GCC were similar in the active and placebo groups in the macula and papillomacular bundle. In the intention to treat comparison, mean adjusted affected eye macular retinal nerve fiber layer thickness at six months was 4.67 μm greater in the active group (a 42% treatment effect). Mean adjusted macular GCC thickness was 5.63 μm greater in the active group (a 28% treatment effect). Treatment had no significant effect on macular GC/IPL when measured alone.
In the papillomacular bundle, mean adjusted retinal nerve fiber layer thickness was 2.49 μm greater in the active group at six months, mean GC/IPL thickness 2.79 μm greater, and mean GCC thickness 5.41 μm greater.
BARCELONA—In addition to its neuroprotective effect on the peripapillary retinal nerve fiber layer, sodium channel blockade with phenytoin also appears to prevent degeneration of the macular ganglion cell complex after acute optic neuritis, according to data presented at the 31st Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS).
Rhian E. Raftopoulos, MbChb, of University College London, and colleagues previously reported in a phase II trial that sodium channel blockade with phenytoin is neuroprotective in acute optic neuritis. The primary outcome measurements were the thickness of the peripapillary retinal nerve fiber layer and macular volume, measured using optical coherence tomography (OCT).
In the present study, the researchers sought to determine whether this neuroprotective effect is selective for particular anatomical layers of the retina. They enrolled patients with acute optic neuritis and randomized them within two weeks of symptom onset to receive phenytoin or placebo for three months. Spectral domain fast macular and papillomacular bundle (PMB) OCT scans were performed at baseline and after six months. Masked automated retinal layer segmentation was performed to obtain average thickness measures of retinal nerve fiber layer, ganglion cell and inner plexiform layer (GC/IPL), and the composite ganglion cell complex. The ganglion cell complex (GCC) encompassed the retinal nerve fiber layer plus GC/IPL. Active versus placebo differences in mean six-month affected eye retinal nerve fiber layer, GC/IPL, and GCC were calculated from macular (n=60) and PMB (n=48) scans, adjusted for the corresponding baseline measurements in the unaffected eye.
At baseline, the mean thicknesses of the retinal nerve fiber layer, GC/IPL, and GCC were similar in the active and placebo groups in the macula and papillomacular bundle. In the intention to treat comparison, mean adjusted affected eye macular retinal nerve fiber layer thickness at six months was 4.67 μm greater in the active group (a 42% treatment effect). Mean adjusted macular GCC thickness was 5.63 μm greater in the active group (a 28% treatment effect). Treatment had no significant effect on macular GC/IPL when measured alone.
In the papillomacular bundle, mean adjusted retinal nerve fiber layer thickness was 2.49 μm greater in the active group at six months, mean GC/IPL thickness 2.79 μm greater, and mean GCC thickness 5.41 μm greater.