The combination of bilateral optic atrophy and homonymous visual field loss usually implies the presence of a lesion of the pregeniculate visual pathways. Typically, this results in temporal atrophy of the optic disc ipsilateral to the lesion and a bow tie atrophy of the contralateral eye. This pattern arises from loss of noncrossing fibers in the ipsilateral eye and the loss of crossing fibers in the contralateral eye (4). The presence of an RAPD in the contralateral eye indicates a lesion of the optic tract, whereas the absence of an RAPD signifies a lesion beyond the point where the pupillomotor fibers leave the optic tract.
OCT can demonstrate thinning of the RNFL in optic tract lesions, but the pattern of RNFL loss does not readily demonstrate a homonymous nature of the lesion. A bow tie pattern of RNFL loss also is not usually apparent. The availability of software to provide segmentation of the retinal layers in the macula allows the analysis of the RGC-IPL complex. Homonymous thinning of the RGC-IPL in a patient with an optic tract lesion due to neuromyelitis optica has been published (11).
Our patient had a right occipital lobe abscess. Both before and after neurosurgical drainage, neuroimaging studies did not detect any abnormality of the optic tracts or lateral geniculate nuclei. The homonymous thinning of the RGC-IPL on OCT exhibited by our patient most likely represents TRD. Interestingly, the peripheral extent of the homonymous ganglion cell-inner plexiform layer thinning (6°) on the probability plot was not as extensive as the visual field defect (16°). Possibly, the central macular fibers near fixation are more likely to show TRD.
In a cohort of patients with autosomal-demonstrated optic atrophy, Rönnbäck et al (13) showed that measurement of RGCL-IPL complex was more sensitive than RNFL thickness in detecting structural loss. The OCT results in our patient support a similar conclusion in patients with TRD due to a retrogeniculate lesion.
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