Jiang Li, Demer Joseph L
Department of Ophthalmology, David Geffen Medical School, University of California, Los Angeles, Los Angeles, California, USA.
Ophthalmology. 2008 Nov;115(11):2079-86. doi: 10.1016/j.ophtha.2008.04.040. Epub 2008 Aug 9.
Biomechanical modeling consistently indicates that superior oblique (SO) muscle weakness alone is insufficient to explain the large hypertropia often observed in SO muscle palsy. Magnetic resonance imaging (MRI) was used to investigate if any size or contractility changes in the inferior rectus (IR) muscle may contribute.
Prospective, case-control study.
Seventeen patients with unilateral SO muscle palsy and 18 orthotropic subjects.
Surface coils were used to obtain sets of contiguous, 2-mm-thick, high-resolution, coronal MRI views in different gazes. Cross-sectional areas of the IR and SO muscles were determined in supraduction and infraduction for evaluation of size and contractility. Diagnosis of SO muscle palsy was based on clinical presentations, subnormal contractility, and SO muscle size less than the normal 95% confidence limit.
Cross-sectional areas of the IR and SO muscles.
Patients had 15.9+/-7.2 prism diopters (Delta; mean+/-standard deviation) of central gaze hypertropia and exhibited ipsilesional SO muscle atrophy and subnormal contractility. Mean ipsilesional, contralesional, and normal IR muscle cross-sections were 28.5+/-3.5 mm(2), 31.9+/-3.8 mm(2), and 31.8+/-5.8 mm(2), whereas mean contractility was 16.5+/-3.8 mm(2), 20.5+/-4.1 mm(2), and 16.6+/-4.8 mm(2), respectively. Ipsilesional IR muscle cross-section and contractility was significantly less than contralesional cross-section and contractility (P<0.01).
In SO muscle palsy, the contralesional IR muscle is larger and more contractile than the ipsilesional IR muscle, reflecting likely neurally mediated changes that augment the relatively small hypertropia resulting from SO muscle weakness alone. Recession of the hyperfunctioning contralesional IR muscle recession in SO muscle palsy is a physiologic therapy.
生物力学模型一直表明，单纯上斜肌（SO）肌无力不足以解释在SO肌麻痹中经常观察到的明显上斜视。使用磁共振成像（MRI）来研究下直肌（IR）肌肉的大小或收缩性变化是否可能起作用。
前瞻性病例对照研究。
17名单侧SO肌麻痹患者和18名正视者。
使用表面线圈在不同注视方向获取连续的、2毫米厚的高分辨率冠状面MRI图像。在眼球上转和下转时确定IR和SO肌肉的横截面积，以评估大小和收缩性。SO肌麻痹的诊断基于临床表现、收缩功能低下以及SO肌大小小于正常95%置信区间。
IR和SO肌肉的横截面积。
患者中央注视上斜视度数为15.9±7.2三棱镜度（Δ；平均值±标准差），患侧SO肌萎缩且收缩功能低下。患侧、对侧和正常IR肌的平均横截面积分别为28.5±3.5平方毫米、31.9±3.8平方毫米和31.8±5.8平方毫米，而平均收缩性分别为16.5±3.8平方毫米、20.5±4.1平方毫米和16.6±4.8平方毫米。患侧IR肌的横截面积和收缩性明显小于对侧的横截面积和收缩性（P<0.01）。
在SO肌麻痹中，对侧IR肌比患侧IR肌更大且收缩性更强，这反映了可能由神经介导的变化，这些变化加剧了仅由SO肌无力导致的相对较小的上斜视。在SO肌麻痹中，对功能亢进的对侧IR肌进行后徙是一种生理性治疗方法。
