Abstract：
BACKGROUND: Convergence insufficiency (CI) is an oculomotor abnormality characterised by exophoria and inadequate convergence when focusing on nearby objects. CI has been shown to cause symptoms when reading. However, the downstream consequences on brain structure have yet to be investigated. Here, we investigated the neural consequences of symptomatic CI, focusing on the left arcuate fasciculus, a bundle of white matter fibres which supports reading ability and has been associated with reading deficits.
METHODS: We compared the arcuate fasciculus microstructure of participants with symptomatic CI versus normal binocular vision (NBV). Six CI participants and seven NBV controls were included in the analysis. All participants were scanned with 3 T magnetic resonance imaging (MRI), and anatomical and diffusion-weighted images were acquired. Diffusion-weighted images were processed with TRACULA to identify the arcuate fasciculus in each participant and compute volume and radial diffusivity (RD).
RESULTS: Compared with NBV controls, those with symptomatic CI had significantly smaller arcuate fasciculi bilaterally (left: t = -3.21, p = 0.008; right: t = -3.29, p = 0.007), and lower RD in the left (t = -2.66, p = 0.02), but not the right (t = -0.81, p = 0.44, false discovery rate (FDR)-corrected p > 0.05) arcuate fasciculus. Those with higher levels of reading symptoms had smaller arcuate fasciculi (r = -0.74, p = 0.004) with lower RD (r = -0.61, p = 0.03).
CONCLUSIONS: These findings suggest that symptomatic CI may lead to microstructural changes in the arcuate fasciculus. Since it is highly unlikely that abnormalities in the arcuate fasciculus are the cause of the neuromuscular deficits in the eyes, we argue that these changes may be a potential neuroplastic consequence of disruptions in sustained reading.
METHODS: We compared the arcuate fasciculus microstructure of participants with symptomatic CI versus normal binocular vision (NBV). Six CI participants and seven NBV controls were included in the analysis. All participants were scanned with 3 T magnetic resonance imaging (MRI), and anatomical and diffusion-weighted images were acquired. Diffusion-weighted images were processed with TRACULA to identify the arcuate fasciculus in each participant and compute volume and radial diffusivity (RD).
RESULTS: Compared with NBV controls, those with symptomatic CI had significantly smaller arcuate fasciculi bilaterally (left: t = -3.21, p = 0.008; right: t = -3.29, p = 0.007), and lower RD in the left (t = -2.66, p = 0.02), but not the right (t = -0.81, p = 0.44, false discovery rate (FDR)-corrected p > 0.05) arcuate fasciculus. Those with higher levels of reading symptoms had smaller arcuate fasciculi (r = -0.74, p = 0.004) with lower RD (r = -0.61, p = 0.03).
CONCLUSIONS: These findings suggest that symptomatic CI may lead to microstructural changes in the arcuate fasciculus. Since it is highly unlikely that abnormalities in the arcuate fasciculus are the cause of the neuromuscular deficits in the eyes, we argue that these changes may be a potential neuroplastic consequence of disruptions in sustained reading.
摘要：
背景：收敛不足（CI）是一种动眼异常，其特征是在聚焦于附近物体时出现外隐和收敛不足。CI已被证明在阅读时引起症状。然而,下游对大脑结构的影响还有待研究。这里,我们研究了症状性CI的神经后果，重点是左弓状束，一束支持阅读能力并与阅读缺陷有关的白质纤维。
方法：我们比较了具有症状性CI和正常双眼视觉（NBV）的参与者的弓形束微结构。分析中包括了SixCI参与者和7名NBV对照。所有参与者均接受3T磁共振成像（MRI）扫描，获取解剖和扩散加权图像。用TRACULA处理扩散加权图像，以识别每个参与者的弓形束，并计算体积和径向扩散率（RD）。
结果：与NBV对照相比，有症状的患者双侧弓状束明显较小（左：t=-3.21，p=0.008；右：t=-3.29，p=0.007），和左侧较低的RD（t=-2.66，p=0.02），但不正确（t=-0.81，p=0.44，错误发现率（FDR）校正p>0.05）弓状束。阅读症状水平较高的患者弓状肌束较小（r=-0.74，p=0.004），RD较低（r=-0.61，p=0.03）。
结论：这些发现提示症状性CI可能导致弓状束的微观结构改变。由于弓状束的异常极不可能是眼睛神经肌肉缺陷的原因，我们认为，这些变化可能是持续阅读中断的潜在神经可塑性后果。
方法：我们比较了具有症状性CI和正常双眼视觉（NBV）的参与者的弓形束微结构。分析中包括了SixCI参与者和7名NBV对照。所有参与者均接受3T磁共振成像（MRI）扫描，获取解剖和扩散加权图像。用TRACULA处理扩散加权图像，以识别每个参与者的弓形束，并计算体积和径向扩散率（RD）。
结果：与NBV对照相比，有症状的患者双侧弓状束明显较小（左：t=-3.21，p=0.008；右：t=-3.29，p=0.007），和左侧较低的RD（t=-2.66，p=0.02），但不正确（t=-0.81，p=0.44，错误发现率（FDR）校正p>0.05）弓状束。阅读症状水平较高的患者弓状肌束较小（r=-0.74，p=0.004），RD较低（r=-0.61，p=0.03）。
结论：这些发现提示症状性CI可能导致弓状束的微观结构改变。由于弓状束的异常极不可能是眼睛神经肌肉缺陷的原因，我们认为，这些变化可能是持续阅读中断的潜在神经可塑性后果。
