Clavagnier Simon, Dumoulin Serge O, Hess Robert F
McGill Vision Research, Department of Ophthalmology, McGill University, Montreal, Quebec H3A 1A1, Canada, and.
Department of Experimental Psychology, University of Utrecht, 3584 CH Utrecht, The Netherlands.
J Neurosci. 2015 Nov 4;35(44):14740-55. doi: 10.1523/JNEUROSCI.1101-15.2015.
The neural basis of amblyopia is a matter of debate. The following possibilities have been suggested: loss of foveal cells, reduced cortical magnification, loss of spatial resolution of foveal cells, and topographical disarray in the cellular map. To resolve this we undertook a population receptive field (pRF) functional magnetic resonance imaging analysis in the central field in humans with moderate-to-severe amblyopia. We measured the relationship between averaged pRF size and retinal eccentricity in retinotopic visual areas. Results showed that cortical magnification is normal in the foveal field of strabismic amblyopes. However, the pRF sizes are enlarged for the amblyopic eye. We speculate that the pRF enlargement reflects loss of cellular resolution or an increased cellular positional disarray within the representation of the amblyopic eye.
The neural basis of amblyopia, a visual deficit affecting 3% of the human population, remains a matter of debate. We undertook the first population receptive field functional magnetic resonance imaging analysis in participants with amblyopia and compared the projections from the amblyopic and fellow normal eye in the visual cortex. The projection from the amblyopic eye was found to have a normal cortical magnification factor, enlarged population receptive field sizes, and topographic disorganization in all early visual areas. This is consistent with an explanation of amblyopia as an immature system with a normal complement of cells whose spatial resolution is reduced and whose topographical map is disordered. This bears upon a number of competing theories for the psychophysical defect and affects future treatment therapies.
弱视的神经基础一直存在争议。有人提出了以下几种可能性:中央凹细胞丧失、皮质放大率降低、中央凹细胞空间分辨率丧失以及细胞图谱的地形紊乱。为了解决这个问题,我们对患有中度至重度弱视的人类中央视野进行了群体感受野(pRF)功能磁共振成像分析。我们测量了视网膜拓扑视觉区域中平均pRF大小与视网膜偏心率之间的关系。结果表明,斜视性弱视患者中央凹视野的皮质放大率正常。然而,弱视眼的pRF大小增大。我们推测,pRF增大反映了弱视眼表征内细胞分辨率的丧失或细胞位置紊乱的增加。
弱视是一种影响3%人群的视力缺陷,其神经基础仍存在争议。我们对弱视参与者进行了首次群体感受野功能磁共振成像分析,并比较了弱视眼和健侧正常眼在视觉皮层的投射。发现弱视眼的投射在所有早期视觉区域都具有正常的皮质放大因子、增大的群体感受野大小和地形紊乱。这与将弱视解释为一个细胞数量正常但空间分辨率降低且地形图紊乱的不成熟系统相一致。这与许多关于心理物理学缺陷的相互竞争的理论相关,并影响未来的治疗方法。