AbstractAcute and chronic vision loss due to neuromyelitis optica (NMO) can be difficult to distinguish from optic neuritis associated with multiple sclerosis (MS) and other causes of visual loss. This is especially true in cases where classic findings of multiple spinal cord level involvement with transverse myelitis is not present and in cases where an IgG1 autoantibody (NMO‐IgG) that binds aquaporin 4 (AQP4) is not present at the time of visual loss. A number of studies have compared features of the inner retina defined by optical coherence tomography (OCT) in NMO and in MS and have found that patients with NMO have much greater axonal loss when matched for final visual acuity at the chronic phase. During acute visual loss, scanning laser polarimetry (SLP‐GDx) is abnormal before changes in OCT features are apparent. This is due to an acute disorganization of axon microfilaments and microtubules that appears to predict final outcome. At the sub‐acute phase (2‐4 weeks), the retinal ganglion cell layer thickness shows thinning before the retinal nerve fiber layer becomes thin. The literature will be reviewed on structural features in the acute, sub‐acute and chronic phases of vision loss in optic neuropathy. Commercial interest