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The anterior visual pathway is frequently affected in multiple sclerosis (MS), but how axonal damage extends from the site of the lesion to neuronal bodies in the retina or lateral geniculate nucleus is poorly understood. Thanks to optical coherence tomography (OCT), it is possible to map and quantify the retrograde diffusion of axonal damage to the retina.1 Lesions in the anterior optic pathway promote significant atrophy of retinal nerve fibre layer (RNFL), which develops in the first 3 months after damage and remains stable after 3 months. Moreover, it has been recently demonstrated that retinal damage in MS is complex and may distinctly affect retinal layers, combining either layer thinning (suggesting the presence of synapse loss and neuronal loss) or layer thickening (suggesting the presence of oedema and inflammation). In fact, the analysis of the ganglion cell/inner plexiform layer (ganglion cell layer (GCL)+inner plexiform layer complex (IPL)) and inner nuclear layer (INL) better correlates with functional disability and prognosis than with RNFL atrophy.2 Acute focal lesions of the optic tracts are infrequently recognised in MS, and they constitute an excellent opportunity to study retrograde axonal degeneration. Previous studies with OCT have shown the homonymous hemimacular atrophy ipsilateral to the optic tract lesion as a specific pattern of retinal atrophy in optic tract lesions,3 with a preferential impact on the GCL.4
A patient with relapsing–remitting MS presented with non-painful, new onset, acute bilateral visual deficit. Automated visual field tests demonstrated non-congruent bilateral homonymous right hemianopsia (figure 1A). Visual acuity (Snellen chart) and colour …
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