屈光参差性与斜视性弱视皮层损害的功能磁共振视网膜脑图对比研究

目的 利用血氧水平依赖性功能磁共振成像视网膜脑图技术,对比研究屈光参差性弱视与斜视性弱视皮层功能损害的发生机制.方法 2009年1-10月,以1.5 T MRI系统分别采集9例健康自愿者、南京军区南京总医院和南京东南眼科医院10例单眼屈光参差性弱视患者和10例单眼斜视性弱视患者对视网膜脑图刺激和6epd空间频率、50%对比度的黑白光点刺激的视觉皮层功能数据,对正常对照组主导眼、屈光参差性弱视组弱视眼及斜视件弱视组弱视眼行单因素方差分析,对屈光参差性弱视组、斜视性弱视组的弱视眼及健眼分别行配对t检验,分析比较屈光参差性弱视组与斜视性弱视组的初、高级视觉皮层功能区损害情况,并对两种类型弱视的初、高级皮层损害进行相关分析.结果 单因素方差分析显示屈光参差性弱视眼平均反应T值在V1、V2、V3、Vp、V7区低于对照组主导眼(P<0.05,P值分别为0.018、0.007、0.002、0.000、0.025),与本组健眼比较结果一致(P<0.05,P值分别为0.035、0.007、0.020、0.009、0.023);斜视性弱视眼反应T值在V1、V2、Vp区低于对照组主导眼(P<0.05,P值分别为0.010、0.007、0.003),在V2、Vp区低于本组健眼(P<0.05,P值分别为0.026、0.009),两种比较结果不一致.屈光参差性弱视眼反应T值在V7区低于斜视性弱视组患眼(P<0.05,P=0.048),其他各区两组弱视患眼反应T值差异无统计学意义(均P>0.05).两种类型弱视高级皮层损害与初级皮层损害无因果关系(P>0.05).结论 屈光参差性弱视与斜视性弱视在初级、高级视觉皮层均存在功能损害,高级视觉皮层的功能损害除因初级皮层损害导致高级皮层激活减低以外,可能还存在更为复杂的神经机制.斜视件弱视在初级视觉皮层除与屈光参差性弱视一样具有视觉神经元的功能损害和(或)神经元之间异常的相瓦作用外,可能还存在健眼对弱视眼的抑制作用;屈光参差性弱视在高级视觉皮层对高空间频率刺激的采集和编码较斜视性弱视减少.

Comparison of deficits in visual cortex between anisometropic and strabismic amblyopia by fMRI retinotopic mapping

Objective To study the neural mechanism of visual cortical deficits between anisometropic and strabismic amblyopia comparatively by BOLD-fMRI retinotopic mapping. Methods Ten anisometropic amblyopes, 10 strabismic amblypes and 9 normal subjects underwent fMRI with retinotopic mapping and luminous spots stimuli (spatial frequency: 6 cpd, contrast; 0.5). 1. 5T MRI system was used to obtain functional images of visual cortex. Responses in primary and secondary visual cortex were compared among the dominant (normal subject group) , anisometropic and strabismic amblyopic eyes by one-way ANOVA, successively analyzed by paired-samples t test between amblyopic eyes and fellow fixing eyes (anisometropic and strabismic amblyopia group respectively) . Their fMRI deficits of amblyopes were analyzed regressively in two amblyopia groups respectively. Results The result of one-way ANOVA showed significantly a lower activation (average T value) in V1, V2, V3, Vp and V7 visual areas (P < 0. 05,P values 0. 018, 0. 007, 0. 002, 0. 000, 0.025 respectively) between anisometropic amblyopia and normal group. This was in accordance with the result of paired-samples t test between amblyopic eyes and fellow fixing eyes in anisometropic amblyopia group (P < 0. 05 , P values 0.035, 0. 007, 0. 020, 0. 009, 0. 023 respectively). Statistical difference was found in V1, V2 and Vp areas between strabismic amblyopia and normal group (P < 0.05, P values 0.010, 0.007 & 0.003 respectively). The paired-samples t test in strabismic amblyopia group showed statistical difference only in V2, Vp areas ( P < 0. 05 , P values 0. 026 and 0. 009 respectively. ). So the two results were discordant. Between the two amblyopic groups, there was no statistical difference (P > 0. 05) except in V7 area (P < 0. 05, P value = 0. 048). There was no causal relation between the primary visual cortical deficits and the secondary cortex in amblyopia ( P > 0. 05 ). Conclusion Anisometropic amblyopia and strabismic amblyopia both have functional deficits in the primary and secondary visual cortex. The neural mechanism of secondary visual cortical deficits may be more complex than decreased cortex activation induced by the deficit of primary cortex. In the primary cortex, strabismic amblyopia and anisometropic amblyopia have neuronal deficits and/or abnormal interaction. In addition, strabismic amblyopia may also have suppressive influences of the fixing eyes upon the amblyopic eyes. Anisometropic amblyopia has the neural undersampling at a high spatial frequency in the secondary visual cortex as compared to amblyopic amblyopia.