Retinal Ganglion Cell Atrophy in Homonymous Hemianopia due to Acquired Occipital Lesions Observed Using Cirrus High-Definition-OCT

Abstract

Purpose. To report a reduction in macular ganglion cell layer and inner plexiform layer (GCL+IPL) thickness and circumpapillary retinal nerve fiber layer (cpRNFL) thickness using spectral-domain optical coherence tomography in patients with homonymous hemianopia due to posterior cerebral artery (PCA) stroke. Methods. Seven patients with PCA stroke were examined using Cirrus high-definition-OCT. The GCL+IPL thicknesses were divided into the hemianopic and unaffected sides. The relationship between the time after stroke and the GCL+IPL thicknesses in the hemianopic side was evaluated. Results. The average thicknesses of the GCL+IPL were 64.6 and 82.0 μm on the hemianopic and unaffected sides, respectively, and the measurement was significantly thinner on the former side (p = 0.018). A regression analysis revealed a negative linear relationship (R 2 = 0.574, p = 0.049) between the time after stoke and the GCL+IPL thicknesses on the hemianopic side. The supratemporal and inferotemporal cpRNFL thicknesses in the eyes ipsilateral to the stroke showed a significant reduction. Conclusion. Our findings confirmed our previous observations that the degeneration of retinal ganglion cells can occur after PCA stroke. GCL+IPL thinning was demonstrated in the hemiretinae corresponding to the affected hemifields. Also, it is suggested that the retinal changes observed are progressive.

Evaluation of Significance Maps and the Analysis of the Longitudinal Time Course of the Macular Ganglion Cell Complex Thicknesses in Acquired Occipital Homonymous Hemianopia Using Spectral-domain Optical Coherence Tomography

“…In these SD-OCT studies, inner retinal thinning was observed in both the peripapillary and macular areas, in accordance with the patients' hemianopic visual field defects. [9][10][11][12][13][14][15][16][17][18] More recently, sweptsource OCT (SS-OCT), which permits even faster scanning, has been used to study inner retinal thinning in homonymous hemianopia. 19 Recent advancements in spectral-domain optical coherence tomography (SD-OCT) has enabled the assessment of the RGC layer and the ganglion cell complex (GCC), which includes the retinal layers from the internal limiting membrane to the inner plexiform layer.…”

Relative Afferent Pupillary Defects in Homonymous Visual Field Defects Caused by Stroke of the Occipital Lobe Using Pupillometer

“…Recently, it has been reported that retinal thinning possibly due to RTSD is present in humans, as determined using OCT in patients with HVFDs due to lesions not involving the optic tract and LGN. 8–10,24,25 In our previous study, we reported that the inner retina corresponding to the blind visual fields demonstrated thinning within a few years after the onset of occipital damage using spectral-domain OCT. 9 Some of the patients who developed a post-geniculate lesion within 1 year of evaluation did not show inner macular thinning by OCT. 26 Meier et al found that the retinal nerve fibre layer of a patient with HVFD due to an occipital lobe abscess was thinned but no RAPD was noted after 2 years. 10 Conversely, small RAPD due to HVFDs has been detected immediately after stroke, when no retinal atrophy should be present.…”

Occipital tip injury with homonymous central scotoma: OCT-NFL and RGC correlation

“…GCL + IPL has been established as a sensitive marker of retinal thinning from acquired damage to the posterior visual pathways 3, 4, 5, 6, 7, 8, 9, 10. This is intuitive, as half of all RGCs exist within the fovea and are responsible for central vision.…”

“…Several distributions of retinal thinning have been described corresponding with homonymous hemianopia or homonymous quadrantanopsia1, 2, 3, 4, 5, 6, 7, 8 , 10 ; however, to our knowledge fewer studies have examined the relatively rare case of isolated macular-involving scotoma from injury to the occipital tip 9 . We describe this pattern of RNFL and retinal ganglion cell (RGC) complex loss from retrograde trans-synaptic neuronal degeneration.…”