视神经束病变的诊断及病因分类。

IF 4.5 Q1 CLINICAL NEUROLOGY
Brain communications Pub Date : 2025-09-19 eCollection Date: 2025-01-01 DOI:10.1093/braincomms/fcaf354
Natalie S Chen, Heather M McDonald, Jonathan Micieli, Edward Margolin
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引用次数: 0

摘要

关于视神经束综合征的现有文献是有限的,视神经束综合征是由视神经束病变引起的。这项回顾性队列研究的目的是阐明不同的临床和影像学表现的视神经束综合征相对于致病病变。研究人群包括2014年至2024年在两家三级神经眼科诊所就诊的所有视束综合征患者。纳入标准是(i)视束综合征相关征象(同向性偏视和/或相对传入瞳孔缺损和/或乳头周围光学相干断层扫描或神经节细胞分析的特征性发现)和(ii)影像学证实的视束病变。通过医疗数据库确定患者记录并进行审查。统计分析临床/影像学表现与病变类型的关系。56例视神经束综合征患者被确诊。平均年龄49.4±16.7岁,女性37例。病因包括占位性病变(25例)、脱髓鞘(11例)、缺血/出血(9例)、非特异性视束萎缩(8例)、围产期损伤(2例)和创伤(1例)。在就诊时,98%的患者(n = 55)出现视野缺损。在这些患者中,20% (n = 11)表现为完全视野丧失,80% (n = 44)表现为部分视野丧失,其中95% (n = 42)表现为不一致,5% (n = 2)表现为一致。在40例同名性偏视患者中,78% (n = 31)表现为不协调缺陷。54例有乳头周围光学相干断层扫描表现的患者中,41% (n = 22)有对侧带状萎缩和同侧沙漏萎缩。在51例可获得资料的患者中,29% (n = 15)有对侧相对传入瞳孔缺损。脱髓鞘病变患者最可能在症状出现2周内出现(P = 0.0180),最不可能出现带状/沙漏萎缩(P = 0.0112)。以往的研究发现视束病变有相当比例的患者会产生一致性同质性偏视,而本研究中的大多数患者表现为非一致性同质性偏视。因此,视束病变应考虑在患者不完整,不协调和微妙的同源缺陷。在这些患者中,应检查乳头周围光学相干断层扫描是否存在带状和沙漏状萎缩,但可能不太常见,特别是在脱髓鞘病因的患者中。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Diagnosis and etiologic classification of optic tract lesions.

Existing literature regarding optic tract syndrome, which arises from lesions affecting the optic tract(s), is limited. The objective of this retrospective cohort study was to elucidate the diverse clinical and imaging manifestations of the optic tract syndrome relative to the causative lesion. The study population comprised of all patients with optic tract syndrome who were seen at two tertiary neuro-ophthalmology practices from 2014 to 2024. Inclusion criteria were (i) signs associated with optic tract syndrome (homonymous hemianopia and/or relative afferent pupillary defect and/or characteristic findings on peripapillary optical coherence tomography or ganglion cell analysis) and (ii) radiographically confirmed optic tract lesion. Patient records were ascertained through medical databases and reviewed. Statistical analysis was performed to identify relationships between clinical/imaging manifestations and lesion type. Fifty-six patients with optic tract syndrome were identified. The mean age was 49.4 ± 16.7 years, and 37 were female patients. Aetiologies included space-occupying lesions (n = 25), demyelination (n = 11), ischaemia/haemorrhage (n = 9), non-specific optic tract atrophy (n = 8), perinatal insult (n = 2) and trauma (n = 1). At presentation, visual field defects were observed in 98% of patients (n = 55). Of these patients, 20% (n = 11) demonstrated complete field loss while 80% (n = 44) demonstrated partial field loss, of which 95% (n = 42) were incongruent and 5% (n = 2) were congruent. Of the 40 patients with homonymous hemianopia, 78% (n  = 31) demonstrated incongruous defects. Of the 54 patients with peripapillary optical coherence tomography findings, 41% (n = 22) had contralateral band atrophy and ipsilateral hourglass atrophy. Of the 51 patients with available data, 29% (n = 15) had contralateral relative afferent pupillary defect. Patients with demyelinating lesions were most likely to present within 2 weeks of symptom onset (P = 0.0180) and least likely to exhibit band/hourglass atrophy (P = 0.0112). In contrast to previous studies that found a significant percentage of optic tract lesions to produce congruent homonymous hemianopia, most patients in this study demonstrated incongruent homonymous hemianopia. As such, optic tract lesions should be considered in patients with incomplete, incongruous and subtle homonymous defects. Peripapillary optical coherence tomography should be examined for the presence of band and hourglass atrophy in these patients but may be less commonly observed, especially in those with a demyelinating aetiology.

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