结论:Riddoch综合征被认为是由初级视觉皮层(V1)受损引起的,通常在血管事件后。这项研究表明,对V1的解剖输入的损害,即,光辐射,会导致模仿Riddoch综合征的选择性视觉缺陷。结果还突出了大细胞和小细胞视觉系统对损伤的敏感性。总的来说,这项研究提供了新的见解,这将提高我们对脑损伤和神经外科手术对视觉通路影响的理解。Riddoch综合征,以感知能力为特征,有意识地,移动的视觉刺激,而不是静态的,与初级视觉皮层(V1)的病变有关。我们在这里介绍YL患者的情况,在肿瘤切除手术后,他的V1幸免,但仍显示出Riddoch综合征的症状。根据我们的测试,我们假设他的V1的大细胞(M)和小细胞(P)输入可能会受到不同的影响。在第一个实验中,YL在进行多模态磁共振成像(MRI)时,在他的盲区中出现了静态和移动的棋盘,包括结构性的,功能,和扩散,在3T获得。在第二个实验中,我们使用心理物理学和高分辨率fMRI评估了YL对M和P视觉刺激的神经反应。我们在他的视觉皮层中发现了广泛的活动,但不是静态的,视觉刺激,而我们的心理物理测试表明,只有低空间频率的移动棋盘被感知。高分辨率功能磁共振成像显示YL的V1对M刺激的反应强烈,对P刺激的反应非常弱,表示影响V1的功能性P损伤。此外,YL经常报告在没有视觉刺激的情况下看到运动刺激并辨别其运动方向,表明他正在经历视觉幻觉。总的来说,这项研究强调了对V1的P输入选择性丢失导致Riddoch综合征和视觉运动幻觉的可能性。
CONCLUSIONS: The Riddoch syndrome is thought to be caused by damage to the primary visual cortex (V1), usually following a vascular event. This study shows that damage to the anatomical input to V1, i.e., the optic radiations, can result in selective visual deficits that mimic the Riddoch syndrome. The results also highlight the differential susceptibility of the magnocellular and parvocellular visual systems to injury. Overall, this study offers new insights that will improve our understanding of the impact of brain injury and neurosurgery on the visual pathways. The Riddoch syndrome, characterised by the ability to perceive, consciously, moving visual stimuli but not static ones, has been associated with lesions of primary visual cortex (V1). We present here the case of patient YL who, after a tumour resection surgery that spared his V1, nevertheless showed symptoms of the Riddoch syndrome. Based on our testing, we postulated that the magnocellular (M) and parvocellular (P) inputs to his V1 may be differentially affected. In a first experiment, YL was presented with static and moving checkerboards in his blind field while undergoing multimodal magnetic resonance imaging (MRI), including structural, functional, and diffusion, acquired at 3 T. In a second experiment, we assessed YL\'s neural responses to M and P visual stimuli using psychophysics and high-resolution fMRI acquired at 7 T. YL\'s optic radiations were partially damaged but not severed. We found extensive activity in his visual cortex for moving, but not static, visual stimuli, while our psychophysical tests revealed that only low-spatial frequency moving checkerboards were perceived. High-resolution fMRI revealed strong responses in YL\'s V1 to M stimuli and very weak ones to P stimuli, indicating a functional P lesion affecting V1. In addition, YL frequently reported seeing moving stimuli and discriminating their direction of motion in the absence of visual stimulation, suggesting that he was experiencing visual hallucinations. Overall, this study highlights the possibility of a selective loss of P inputs to V1 resulting in the Riddoch syndrome and in hallucinations of visual motion.