Gräf Michael, Weihs Johannes
Department of Ophthalmology, Justus-Liebig-University of Giessen, Friedrichstrasse 18, 35392, Giessen, Germany.
Graefes Arch Clin Exp Ophthalmol. 2009 Feb;247(2):253-9. doi: 10.1007/s00417-008-0950-0. Epub 2008 Sep 23.
Monocular occlusion eliminates the stimulus for fusional vergence. Diagnostic occlusion may therefore be helpful in isolating the genuine profile of the fundamental ocular motility disorder, which may be an important finding regarding both differential diagnosis of strabismus and dosage of surgery. We investigated the effect of diagnostic occlusion on the motility pattern of acquired trochlear nerve palsy.
Forty-eight patients aged between 6 and 78 years (median 49 years) with unilateral trochlear nerve palsy were first examined without patching, and then after 3 days of diagnostic occlusion. The onset of palsy was 1-35 years before (median 2 years). Squint angles localized with a dark red glass in front of the non-paretic eye were measured at a distance of 2.5 m, using the Harms tangent screen. Vertical and cyclotorsional angles in primary position (PP), 25 degrees abduction of the non-paretic eye (adduction of the paretic eye), and 25 degrees downgaze were measured.
The relation between hyperdeviation of the paretic eye and excyclodeviation (medians of the angles in degrees, ranges in brackets) before and after diagnostic occlusion was 5/5 and 4/6 (0;14/-1;10 and 0;19/2;13) in PP. In contralateral gaze, the relation was 8/5 and 8/6 (0;21/0;10 and 1;24/1;15), and in downgaze, 10/7 and 8/8 (0;21/1;14 and 0;23/3;18). The increase in excyclodeviation, though statistically significant (in PP, p = 0.0002) was small, with a median of 1 degree and large variability. The decrease in hyperdeviation was statistically significant in downgaze. The head-tilt phenomenon remained unchanged.
In patients with trochlear nerve palsy, diagnostic occlusion regularly causes an increase in excyclodeviation. In 25% of patients, this increase exceeds 3 degrees. The more variable change in vertical deviation, and the lack in change in the head-tilt phenomenon, can be explained by the fact that central gain-modulation causing an increase in both vertical deviation and the head-tilt phenomenon is not reversible within the relatively short time of 3 days. Diagnostic occlusion can eliminate compensatory innervation and may thereby release the genuine motility pattern, but the occlusion can also induce artificial squint angles.
单眼遮盖消除了融合性集合的刺激。因此,诊断性遮盖可能有助于分离出基本眼球运动障碍的真实情况,这对于斜视的鉴别诊断和手术剂量可能是一个重要发现。我们研究了诊断性遮盖对后天性滑车神经麻痹眼球运动模式的影响。
48例年龄在6至78岁(中位年龄49岁)的单侧滑车神经麻痹患者,首先在未遮盖的情况下进行检查,然后在诊断性遮盖3天后再次检查。麻痹的发病时间为1至35年前(中位时间2年)。使用哈姆斯正切屏,在2.5米的距离测量非麻痹眼前放置深红色玻璃时确定的斜视角度。测量了原在位(PP)、非麻痹眼外展25度(麻痹眼内收)和下视25度时的垂直和旋转斜视角度。
诊断性遮盖前后,麻痹眼上斜视与外旋转斜视之间的关系(角度中位数,括号内为范围)在PP位为5/5和4/6(0;14/-1;10和0;19/2;13)。在对侧注视时,关系为8/5和8/6(0;21/0;10和1;24/1;15),在下视时,为10/7和8/8(0;21/1;14和0;23/3;18)。外旋转斜视的增加虽然具有统计学意义(在PP位,p = 0.0002),但幅度较小,中位数为1度且变异性较大。下视时上斜视的减少具有统计学意义。头倾现象保持不变。
在滑车神经麻痹患者中,诊断性遮盖通常会导致外旋转斜视增加。25%的患者中,这种增加超过3度。垂直偏差变化的更大变异性以及头倾现象缺乏变化,可以用以下事实来解释:在相对较短的3天时间内,导致垂直偏差和头倾现象增加的中枢增益调节是不可逆的。诊断性遮盖可以消除代偿性神经支配,从而可能释放真实的眼球运动模式,但遮盖也可能诱发人为的斜视角度。