PDF(Pubmed)
Abstract：
BACKGROUND: Disconjugate eye movements are essential for depth perception in frontal-eyed species, but their underlying neural substrates are largely unknown. Lesions in the midbrain can cause disconjugate eye movements. While vertically disconjugate eye movements have been linked to defective visuo-vestibular integration, the pathophysiology and neuroanatomy of horizontally disconjugate eye movements remains elusive.
METHODS: A patient with a solitary focal midbrain lesion was examined using detailed clinical ocular motor assessments, binocular videooculography and diffusion-weighted MRI, which was co-registered to a high-resolution cytoarchitectonic MR-atlas.
RESULTS: The patient exhibited both vertically and horizontally disconjugate eye alignment and nystagmus. Binocular videooculography showed a strong correlation of vertical and horizontal oscillations during fixation but not in darkness. Oscillation intensities and waveforms were modulated by fixation, illumination, and gaze position, suggesting shared visual- and vestibular-related mechanisms. The lesion was mapped to a functionally ill-defined area of the dorsal midbrain, adjacent to the posterior commissure and sparing nuclei with known roles in vertical gaze control.
CONCLUSIONS: A circumscribed region in the dorsal midbrain appears to be a key node for disconjugate eye movements in both vertical and horizontal planes. Lesioning this area produces a unique ocular motor syndrome mirroring hallmarks of developmental strabismus and nystagmus. Further circuit-level studies could offer pivotal insights into shared pathomechanisms of acquired and developmental disorders affecting eye alignment.
METHODS: A patient with a solitary focal midbrain lesion was examined using detailed clinical ocular motor assessments, binocular videooculography and diffusion-weighted MRI, which was co-registered to a high-resolution cytoarchitectonic MR-atlas.
RESULTS: The patient exhibited both vertically and horizontally disconjugate eye alignment and nystagmus. Binocular videooculography showed a strong correlation of vertical and horizontal oscillations during fixation but not in darkness. Oscillation intensities and waveforms were modulated by fixation, illumination, and gaze position, suggesting shared visual- and vestibular-related mechanisms. The lesion was mapped to a functionally ill-defined area of the dorsal midbrain, adjacent to the posterior commissure and sparing nuclei with known roles in vertical gaze control.
CONCLUSIONS: A circumscribed region in the dorsal midbrain appears to be a key node for disconjugate eye movements in both vertical and horizontal planes. Lesioning this area produces a unique ocular motor syndrome mirroring hallmarks of developmental strabismus and nystagmus. Further circuit-level studies could offer pivotal insights into shared pathomechanisms of acquired and developmental disorders affecting eye alignment.
摘要：
背景：非共轭眼动对于额眼物种的深度感知至关重要，但是它们潜在的神经底物在很大程度上是未知的。中脑的病变可引起非共轭眼球运动。虽然垂直非共轭的眼球运动与前庭整合缺陷有关，水平非共轭眼球运动的病理生理学和神经解剖学仍然难以捉摸。
方法：使用详细的临床眼运动评估对患有孤立性局灶性中脑病变的患者进行检查，双目图像成像和弥散加权磁共振成像，已与高分辨率细胞结构MR图谱共同注册。
结果：患者表现出垂直和水平非共轭眼睛对齐和眼球震颤。双目视频眼睛照相术显示，在固定过程中垂直和水平振荡之间存在很强的相关性，但在黑暗中却没有。振荡强度和波形由固定调制，照明,和凝视位置，提示共同的视觉和前庭相关机制。病变被映射到背侧中脑功能不明确的区域，邻近后连合和保留核，在垂直凝视控制中具有已知作用。
结论：背侧中脑的外接区域似乎是垂直和水平平面上不共轭眼球运动的关键节点。损伤该区域会产生独特的眼运动综合征，反映出发育性斜视和眼球震颤的标志。进一步的电路水平研究可以为影响眼睛对准的获得性和发育障碍的共同病理机制提供关键见解。
方法：使用详细的临床眼运动评估对患有孤立性局灶性中脑病变的患者进行检查，双目图像成像和弥散加权磁共振成像，已与高分辨率细胞结构MR图谱共同注册。
结果：患者表现出垂直和水平非共轭眼睛对齐和眼球震颤。双目视频眼睛照相术显示，在固定过程中垂直和水平振荡之间存在很强的相关性，但在黑暗中却没有。振荡强度和波形由固定调制，照明,和凝视位置，提示共同的视觉和前庭相关机制。病变被映射到背侧中脑功能不明确的区域，邻近后连合和保留核，在垂直凝视控制中具有已知作用。
结论：背侧中脑的外接区域似乎是垂直和水平平面上不共轭眼球运动的关键节点。损伤该区域会产生独特的眼运动综合征，反映出发育性斜视和眼球震颤的标志。进一步的电路水平研究可以为影响眼睛对准的获得性和发育障碍的共同病理机制提供关键见解。
