Rabin Jeff, Kryder Andrew, Lam Dan
The Rosenberg School of Optometry, University of the Incarnate Word, San Antonio, Texas, USA.
Clin Exp Optom. 2018 Jan;101(1):69-72. doi: 10.1111/cxo.12567. Epub 2017 Jun 21.
Neural compensatory mechanisms have been proposed, which preserve the binocular visual field in glaucoma, as well as cognition in Alzheimer's disease and motor function in Parkinson's disease. It is conceivable that comparable mechanisms operate to preserve function in congenital and/or dystrophic disease. In hereditary colour vision deficiency (CVD), we observed significant facilitation in the amplitude of the binocular cone-specific visual evoked potential (VEP) compared to the monocular amplitude for the cone type corresponding to the CVD. We propose that this finding may reflect preservation of function in hereditary colour vision deficiency.
Binocular and monocular L, M and S cone-specific VEPs were recorded from 12 colour vision deficient subjects and 17 with normal colour vision, confirmed to be CVD or normal on a battery of colour vision tests. Binocular VEP amplitudes were compared to monocular amplitudes within subjects and between subject groups.
Subjects with CVDs showed binocular facilitation of VEP amplitude (enhancement more than 2.0 times; mean: 2.8 times, p = 0.0003) for the cone type corresponding to their CVD. Mean facilitation of 2.8 times exceeded binocular enhancement for other cone types within CVDs (2.8 times versus 1.2 times) and compared to colour vision normals (2.8 times versus 1.2 times).
Hereditary CVDs show binocular facilitation of cone VEP signals for the cone type corresponding to their CVD. As CVD is typically assessed with foveal stimuli, our findings using wider-field binocular stimulation suggest that enhanced colour perception may occur in CVD across a more extensive area of visual field. These results may relate to binocular visual field enhancement in glaucoma and improved colour vision in CVD at supra-threshold levels of stimulation.
已经提出了神经代偿机制,该机制可保留青光眼患者的双眼视野、阿尔茨海默病患者的认知能力以及帕金森病患者的运动功能。可以想象,类似的机制也在先天性和/或营养不良性疾病中发挥作用以保留功能。在遗传性色觉缺陷(CVD)中,我们观察到与对应于CVD的视锥类型的单眼振幅相比,双眼视锥特异性视觉诱发电位(VEP)的振幅有显著增强。我们认为这一发现可能反映了遗传性色觉缺陷中功能的保留。
对12名色觉缺陷受试者和17名色觉正常受试者进行双眼和单眼L、M和S视锥特异性VEP记录,通过一系列色觉测试确定为CVD或正常。比较受试者内部和受试者组之间的双眼VEP振幅与单眼振幅。
患有CVD的受试者在对应于其CVD的视锥类型上表现出VEP振幅的双眼增强(增强超过2.0倍;平均:2.8倍,p = 0.0003)。平均2.8倍的增强超过了CVD中其他视锥类型的双眼增强(2.8倍对1.2倍),并与色觉正常者相比(2.8倍对1.2倍)。
遗传性CVD在对应于其CVD的视锥类型上表现出视锥VEP信号的双眼增强。由于CVD通常使用中央凹刺激进行评估,我们使用更宽视野双眼刺激的研究结果表明,在CVD中,超过阈值刺激水平时,更广泛的视野区域可能会出现增强的颜色感知。这些结果可能与青光眼患者的双眼视野增强以及CVD患者在超阈值刺激水平下改善的色觉有关。