We read with interest the article by Shin and Demer. We would like to make the following observations and queries, addressing some of which may shed more light on the interesting concept of superior oblique (SO) compartmentalization.
The authors have included subjects from an ongoing study who were determined to have unilateral SO palsy based on ipsilateral reduction of maximum SO cross section on quasi-coronal magnetic resonance imaging (MRI). How were the criteria for inclusion defined? How much reduction in cross-section of SO was considered sufficient for inclusion? Were these apparently reduced SO volumes determined after comparison with fellow eyes, and if yes, how were subjects with bilateral/masked bilateral palsies factored in? Also, the symptom duration of SO palsy was 57.7 ± 43.1 months (range: 2–120 months). Presumably, the extent of reduction of SO cross sections (representing atrophy) would be very heterogeneous in a group with such a wide range of symptom duration, with more atrophy in subjects with longer symptom duration. Subjects with longer symptom duration may also have spread of comitance, which would significantly alter their clinical picture, as will be discussed later.
According to the authors, anisotropic atrophy may represent either medial or lateral compartmental palsy, which cannot be differentiated based on currently available MRI techniques. This may be considered a major limitation of the study vis-à-vis a similar study by Clark and Demer on lateral rectus compartmentalization where it was possible to differentiate superior vs inferior compartment palsy based on MRI.
As the medial compartment inserts anteriorly near the globe equator and the lateral compartment inserts posteriorly, they determine torsional and vertical actions of SO, respectively. Thus, in the present study, in subjects with isotropic atrophy both would be affected. In subjects with anisotropic atrophy, either torsion or vertical deviation would be predominantly affected, not both. Owing to the heterogeneity in the anisotropic group, it is difficult to draw logical conclusions regarding differences in vertical deviation and torsion between the 2 groups. For example, it is difficult to explain why the mean excyclotorsion is more in the anisotropic group when some patients may in fact be having lateral compartment paresis with no or minimal effects on torsion, as compared to the isotropic group where all subjects must have some torsional changes. Also, the authors make no comment on pattern strabismus and how it varies between the 2 groups.
The clinical picture in SO palsy is determined not just by the degree of SO underaction. On the contrary, ipsilateral inferior oblique (IO) overaction, ipsilateral superior rectus overaction, contralateral inferior rectus overaction, and pseudo-overaction of contralateral SO, which develop with spread of comitance, are more important determinants. Thus differences in torsion and vertical deviations seen between the 2 groups may be due to variability in these factors rather than compartmental involvement of SO. The authors have not commented on the degree of IO overaction seen in the 2 groups, as well as on force duction tests for vertical recti, which would help us better understand the clinical picture.
As regards etiology, as the distribution of congenital palsy was equal in both groups, it is difficult to hypothesize which lesions are likely to give rise to compartmental involvement vis-à-vis uniform SO involvement. This probably diminishes the clinical significance of the findings on MRI, as SO atrophy on MRI is not a sine qua non for SO palsy and SO palsy is to be diagnosed not just by fulfillment of the 3-step test but by an amalgamation of clinical findings.