Abstract

The objective of this study was to determine whether transneuronal retrograde degeneration (TRD) of the retinal ganglion cells (RGCs) could be detected by optical coherence tomography (OCT) in humans with lesions other than of the occipital lobe or visual cortex. In addition, whether laterality and severity of retinal nerve fiber layer (RNFL) damage correlated with 3 other variables was determined: laterality of hemispheric damage, arterial territory of infarct, and age of infarct. Cross-sectional, case-control design. Forty-six patients with cerebral ischemic infarction diagnosed based on brain magnetic resonance imaging and 46 normal controls were enrolled. All subjects underwent a complete ophthalmic examination including OCT. Cerebral infarction was categorized by arterial territory: anterior cerebral artery (ACA), middle cerebral artery (MCA), and posterior cerebral artery (PCA). Eyes on the same side of the infarction were referred to as ipsilateral eyes, and eyes on the opposite side of the infarction were referred as contralateral eyes. Retinal nerve fiber layer thickness. Average, superior, temporal, inferior, and nasal RNFL thicknesses were different significantly between patients with cerebral infarction and normal controls. The RNFL thicknesses were reduced significantly at the superior, inferior, and nasal quadrants in the contralateral eyes and at the superior, inferior, and temporal quadrants in the ipsilateral eyes. The RNFL thickness reduction was greater in patients with PCA infarction, followed by MCA and ACA infarction, respectively. Factors related to the average RNFL thickness were time after stroke onset and infarction territory based on both univariate (P = 0.027 and P = 0.046, respectively) and multivariate (P = 0.036 and P = 0.047, respectively) analysis. Retinal nerve fiber layer thickness was reduced in patients with cerebral infarction, providing evidence for TRD of the RGCs. Transneuronal retrograde degeneration was more pronounced in the nasal nerve fiber layer of the contralateral side and in the temporal nerve fiber layer of the ipsilateral side of cerebral damage. The author(s) have no proprietary or commercial interest in any materials discussed in this article.

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