2020 Fiscal Year Final Research Report

Analysis of retinal ganglion cell atrophy and location of cerebral lesions in homonymous hemianopia

Research Project

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Project/Area Number	17K11497
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	Ophthalmology
Research Institution	Kawasaki Medical School
Principal Investigator	Miki Atsushi 川崎医科大学, 医学部, 教授 (90447607)
Co-Investigator(Kenkyū-buntansha)	山下力川崎医療福祉大学, リハビリテーション学部, 准教授 (00515877)
Project Period (FY)	2017-04-01 – 2021-03-31
Keywords	網膜神経節細胞 / 同名半盲 / 後頭葉 / 外側膝状体 / 光干渉断層計 / 視放線 / 標準脳 / 網膜神経線維層
Outline of Final Research Achievements	Inner retinal thinning corresponding to visual field defects is observed using OCT after occipital lobe lesions, but it is controversial whether this change is retinal ganglion cell (RGC) degeneration that occurs beyond the lateral geniculate nucleus. Therefore, based on the brain MRI images of the homonymous hemianopia patients, the responsible lesion was drawn on the standard brain and group data analysis was performed. First, the site of brain damage that contributes to the decrease in retinal thickness in the early stage after the onset of brain damage is the region near the optic tract / lateral geniculate nucleus, and the possibility of direct RGC damage was considered. On the other hand, the site of brain damage in patients with inner retinal thinning in the chronic phase was concentrated in the posterior pole of the occipital lobe. That is, we obtained findings suggesting that trans-synaptic degeneration of RGC beyond the lateral geniculate nucleus may occur.
Free Research Field	神経眼科学
Academic Significance and Societal Importance of the Research Achievements	後天性後頭葉病変の影響が眼球の網膜にまで及ぶとはこれまで考えられていなかったが、最近の光干渉断層計を用いた眼底の定量解析で、後頭葉病変を持つ同名半盲患者では、視野欠損部に一致する網膜内層の菲薄化が見られることが明らかになった。この変化のメカニズムには、網膜神経節細胞の軸索（神経線維）の直接の障害と、外側膝状体のシナプスを越える遠隔作用の両者が存在すると考えられる。後頭葉障害後、数年で網膜内層に萎縮性変化が出ることから、同名半盲の患者において、視機能回復を得るためには、障害部の治療に加えて、発症後数年以内の網膜内層に変化が出現する時期以前に、前部視路（網膜）への逆行性変性を阻止する必要がある。