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症状性集合不足的神经后果:一项小样本研究。

Neural consequences of symptomatic convergence insufficiency: A small sample study.

机构信息

Department of Psychology, The Ohio State University, Columbus, Ohio, USA.

College of Optometry, The Ohio State University, Columbus, Ohio, USA.

出版信息

Ophthalmic Physiol Opt. 2024 May;44(3):537-545. doi: 10.1111/opo.13303. Epub 2024 Mar 21.

DOI:10.1111/opo.13303
PMID:38515331
Abstract

INTRODUCTION

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.

摘要

引言

集合不足(CI)是一种眼动异常,其特征为在注视近物时出现外斜视和会聚不足。CI 已被证明会在阅读时引起症状。然而,其对大脑结构的下游影响尚未得到研究。在这里,我们研究了有症状的 CI 的神经后果,重点关注支持阅读能力的白质束——左弓状束,该束已与阅读缺陷有关。

方法

我们比较了有症状的 CI 患者与正常双眼视力(NBV)患者的弓状束微观结构。分析纳入了 6 名 CI 患者和 7 名 NBV 对照者。所有参与者均接受 3T 磁共振成像(MRI)扫描,并采集解剖和弥散加权图像。使用 TRACULA 处理弥散加权图像,以识别每位参与者的弓状束,并计算体积和放射状弥散系数(RD)。

结果

与 NBV 对照组相比,有症状的 CI 患者双侧的弓状束明显较小(左侧:t=-3.21,p=0.008;右侧:t=-3.29,p=0.007),左侧的 RD 较低(t=-2.66,p=0.02),而右侧的 RD 无差异(t=-0.81,p=0.44,经 FDR 校正后 p>0.05)。阅读症状水平较高的患者,其弓状束较小(r=-0.74,p=0.004),RD 也较低(r=-0.61,p=0.03)。

结论

这些发现表明,有症状的 CI 可能导致弓状束的微观结构变化。由于弓状束异常极不可能是眼肌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引起的潜在神经可塑性后果。

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