Visual Field Defects and Retinal Changes due to Cortical Disorders

DOI
  • Yamashita Tsutomu
    Department of Sensory Science，Faculty of Health Science and Technology，Kawasaki University of Medical Welfare Department of Ophthalmology，Kawasaki Medical School
  • Miki Atsushi
    Department of Sensory Science，Faculty of Health Science and Technology，Kawasaki University of Medical Welfare Department of Ophthalmology，Kawasaki Medical School

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  • 大脳皮質障害による視野異常と網膜の変化

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Abstract

It is generally believed that patients with homonymous hemianopia caused by retrogeniculate lesions do not show any funduscopic abnormality, and that damage to retinal ganglion cells (RGCs) beyond the synapse at the lateral geniculate nucleus does not occur in such patients. We treated patients with homonymous hemianopia following unilateral posterior cerebral artery (PCA) infarction and evaluated their macular ganglion cell complex (GCC) thicknesses. Our findings suggest that the degeneration of the RGCs in the retina, which corresponds to the homonymous hemianopia, can occur within a few years after PCA infarction. It is also indicated that the evaluation of the macular GCC may be superior to the evaluation of the circumpapillary retinal nerve fiber layer for the detection of nerve fiber damage in homonymous hemianopia. The ganglion cell layer, inner plexiform layer, and GCC were significantly thinner on the hemianopic side of the patients with cerebral artery stroke than on the unaffected side and in normal subjects. An area analysis revealed striking thinning in the most central part of the macula, close to the fovea. A regression analysis revealed a negative linear relationship between the time after stroke and the inner retinal thicknesses on the hemianopic side. Moreover, the significance and deviation maps of the abnormal area, as well as the GCC thicknesses, on the hemianopic side significantly correlated with the visual field defects. Furthermore, during the long-term follow-up of the retinal thickness in patients with hemianopia and lesions limited to the posterior pole of the occipital lobe, although changes were not observed immediately after the onset of the brain lesion, hemianopic thinning became apparent a few years later. These findings can be explained by the presence of the trans-synaptic retrograde degeneration of RGCs and their fibers. However, PCA infarction may directly affect the axons of the RGCs in the anterior visual pathways.

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